The exposomal imprint on rosacea: More than skin deep

Abstract

Rosacea is a chronic, inflammatory dermatosis driven by a complex interplay of genetic, environmental and lifestyle factors, collectively known as the exposome. This review explores how intrinsic contributors such as genetic susceptibility, immune dysregulation, microbiome alterations, hormonal influences and psychosocial stress intersect with extrinsic triggers like ultraviolet radiation (UVR), air pollution, dietary factors, and climate variability to shape rosacea pathogenesis. Recent advances in single‐cell transcriptomics have identified fibroblasts as key components of inflammatory and vascular pathways in rosacea. Concurrently, discoveries in non‐coding RNAs and RNA modifications reveal subtype‐specific molecular signatures and novel biomarkers. Mendelian randomization (MR) studies further reveal causal links between rosacea and autoimmune, metabolic and gastrointestinal comorbidities—that rosacea is more than skin deep. The role of the gut–skin axis, particularly involving small intestinal bacterial overgrowth (SIBO) and Helicobacter pylori infection, reflects the importance of microbial and neuroimmune crosstalk. Disparities in diagnosis and management persist, particularly among individuals with skin of colour (SOC) and those with limited healthcare access. By integrating an exposomal framework, this review advocates for a paradigm shift in rosacea management: from reactive treatment to proactive, exposome‐informed intervention. Personalized skincare, microbiome‐targeted strategies, dietary modulation and psychosocial support represent emerging pillars in a holistic, precision medicine framework. Future research should prioritize exposome‐informed prevention, inclusive care models, and the development of personalized interventiouns that address both cutaneous and systemic facets of rosacea.

Rosacea reflects systemic and environmental interactions, not just a skin disorder. Key factors include environmental triggers, genetic and microbiome influences, diagnostic gaps in skin of colour and social determinants. Advances in multi‐omics and exposome integration highlight pathways towards precision medicine, prevention and equitable, patient‐centred care.

Why was the study undertaken?

To clarify rosacea's multifactorial pathogenesis by integrating genetic, molecular, microbial and environmental factors within an exposome framework, highlighting systemic associations and unmet needs in prevention and care

What does this study add?

It identifies fibroblasts, non‐coding RNAs, and transcriptomic signatures as key molecular drivers, while Mendelian randomization uncovers causal links with systemic comorbidities, reframing rosacea as an exposome‐driven disorder extending beyond the skin.

What are the implications of this study for disease understanding and/or clinical care?

The study supports a shift towards proactive, exposome‐informed precision care, including microbiome‐targeted therapies, dietary modulation and psychosocial support, while addressing disparities in diagnosis and treatment, especially among individuals with skin of colour.

INTRODUCTION

Rosacea is a chronic inflammatory skin condition influenced by environmental, dietary, genetic and lifestyle factors that play a critical role in its onset and exacerbation. Hallmark clinical features include skin sensitivity, flushing, centrofacial erythema, telangiectasia, papules, pustules and sebaceous gland hyperplasia. ¹ Four sub‐phenotypes of rosacea have historically been described: erythematotelangiectatic (ETR), papulopustular (PPR), phymatous (PhR) and ocular rosacea, though overlap is common. ² Beyond dermatologic manifestations, rosacea is associated with multiple systemic comorbidities, including hypertension, dyslipidaemia, inflammatory bowel disease (IBD), anxiety and depression. ³ Understanding the exposomal factors implicated in the pathogenesis and exacerbation of rosacea is critical for holistic and personalized patient management. ⁴ The exposome can be defined as the measure of all the exposures of an individual during their lifetime and how these exposures relate to well‐being. ⁵ The external environmental exposures (external exposome) to which an individual is exposed before and after conception, and their consequences at the organ and cellular level (internal exposome), are examined to explain the onset, development and exacerbations of inflammatory diseases like rosacea (Figure 1). ⁶ , ⁷

FIGURE 1.

Integrated exposomal model of rosacea pathogenesis. This figure illustrates the interplay between the totality of exposomal factors affecting rosacea. Intrinsic exposome includes genetic predisposition, immune dysregulation, microbiome alterations, hormonal influences and psychological distress. Extrinsic exposomal factors encompass environmental triggers like ultraviolet radiation (UVR), air pollution, climate change, occupational exposures as well as diet and lifestyle factors like nutrition, alcohol consumption, smoking and skincare practices. These diverse factors converge on shared neurovascular and immune pathways, resulting in characteristic rosacea symptoms. The model also incorporates the influence of social determinants of health (SDOH), such as healthcare access, skin of colour (SOC) underdiagnosis and socio‐economic status, and highlights the impact of digital misinformation in shaping disease perception and self‐management. All figures were created in BioRender (6/9/2025) https://BioRender.com/45wv9jx.

ROSACEA PATHOPHYSIOLOGY

Rosacea is characterized by a complex interplay between skin barrier dysfunction, dysregulated innate and adaptive immune responses, vasodilation and neuroinflammation, mediating the characteristic manifestations of the disease. ⁸ , ⁹ Central to rosacea's pathogenesis is the upregulation of Toll‐like receptor 2 (TLR2), protease activator 2 (PAR2), kallikrein 5 (KLK5) and the antimicrobial peptide LL‐37, namely the TLR2/KLK5/LL‐37 axis. In rosacea skin, this pathway is over‐activated, leading to increased cathelicidin peptides, especially LL‐37, which exhibit vasoregulatory and proangiogenic properties, including cytokine release, leukocyte chemotaxis and matrix metalloproteinase (MMP) activation (notably MMP‐9), contributing to tissue remodelling and inflammation ¹⁰ , ¹¹ , ¹² , ¹³ , ¹⁴ , ¹⁵ (Table 1).

TABLE 1.

Key pathways in rosacea pathophysiology and relevant genes.

Pathophysiological pathway	Key mechanisms/molecular players	Relevant genes/genetic associations
Innate Immune Dysregulation (TLR2/KLK5/LL‐37 axis)	Overactivation of TLR2 → ↑ KLK5 activity → ↑ Cathelicidin LL‐37 → vasodilation, leukocyte chemotaxis, cytokine release, MMP activation (notably MMP‐9)	TLR2, PAR2 (F2RL1), KLK5, CAMP (LL‐37), MMP9
Neurovascular and Neurogenic Inflammation	Environmental triggers (UV, heat, spicy food) activate TRP channels → neuropeptide (Substance P, CGRP) release → mast cell degranulation → ↑ VEGF, histamine, fibroblast growth factors	TRPA1, TRPV1, TRPV4, CALCA (CGRP), VEGFA, PTGDS
Fibroblast‐mediated crosstalk and vascular response	Fibroblasts interact with T cells, macrophages, keratinocytes → inflammatory mediator release; PTGDS upregulated in lesions; contributes to vasodilation	PTGDS, fibroblast signalling networks
Skin barrier dysfunction and keratinocyte signalling	TRP channel dysfunction → impaired Ca2+ homeostasis → abnormal differentiation/lipid synthesis; STAT3 activation in keratinocytes → cytokines → STAT1 activation in immune cells	TRPV1/TRPV4, STAT3, STAT1
Sebaceous gland dysfunction and microbial dysbiosis	Sebocyte dysregulation via TLR2/4; altered sebum composition; sebocytes secrete cytokines/chemokines (CXCL8, CXCL10, IL‐1β, IL‐6 and CCL5)	TLR2, TLR4, CXCL8 (IL‐8), CXCL10, IL1B, IL6, CCL5 and LEP (leptin)
Oxidative stress and ROS detoxification	Excessive ROS from UV exposure and neutrophil activation; impaired antioxidant defences; ↑ GST expression; null GST genotypes associated with risk	GSTT1, GSTM1, GSTP1
Genetic susceptibility and autoimmune links	Shared loci with autoimmune diseases; GWAS identified SNP rs763035 and HLA associations; IRF4, IL13 implicated; VEGF +405 C/G polymorphism; VDR and NOD2 polymorphisms linked to subtypes	HLA‐DRB1, HLA‐DQB1, HLA‐DQA1, IRF4, IL13, VEGFA (+405 C/G), NOD2/CARD15 (R702W), VDR (BsmI), SLC45A2, LRRC4, SH3PXD2A, SLC26A8
Gut–skin axis and immune crosstalk	Dysbiosis (e.g. SIBO), systemic inflammation, neuroimmune modulation; bidirectional links with IBD	NOD2, HLA‐linked immune pathways

Environmental triggers such as UVR, heat and spicy foods activate transient receptor potential (TRP) channels. These include TRPA1, TRPV1 and TRPV4, which are expressed on keratinocytes, endothelial, immune and neuronal cells of rosacea patients. ¹⁶ , ¹⁷ This results in neurogenic inflammation, substance P and calcitonin gene‐related peptide (CGRP) release, mast cell (MC) degranulation, and further upregulation of LL‐37. ¹⁸ , ¹⁹ , ²⁰ MCs release histamine, fibroblast growth factor and vascular endothelial growth factor (VEGF), which is increased in lesional rosacea skin and contributes to vasodilation and neovascularization. ²¹ , ²² , ²³ Fibroblasts are now recognized as key orchestrators of rosacea inflammation. Single‐cell RNA‐sequencing studies revealed that fibroblasts mediate crosstalk between T cells, macrophages, vascular muscle cells, keratinocytes and endothelial cells, initiating and sustaining inflammatory and vascular responses. In mouse models, inhibition of fibroblast activity and prostaglandin D2‐producing (PTGDS) enzyme (upregulated in lesions) reduced the development of rosacea‐like phenotypes and improved vasodilation. ²⁴

Rosacea patients frequently exhibit dry skin (xerosis) and barrier impairment. Abnormal TRP channel function disrupts calcium ion homeostasis, affecting epidermal differentiation and lipid synthesis. A compromised barrier can activate STAT3 signalling in keratinocytes, leading to cytokine release and subsequent STAT1 activation in immune cells, creating a self‐amplifying inflammatory loop. ²⁵ Although classically not associated with seborrhea, rosacea features sebaceous gland dysfunction. Inflammatory cues, through TLR2/TLR4 activation, microbial dysbiosis (notably Demodex folliculorum overgrowth) and neuroendocrine stimuli, alter sebocyte activity. Sebum from rosacea skin displays a higher ratio of myristic acid and lower levels of long‐chain saturated fatty acids, compromising the barrier and promoting inflammation. ²⁶ Sebocytes become immune‐competent, produce cytokines and chemokines, including C–X–C motif chemokine ligand CXCL‐8, CXCL‐10, IL‐1β, IL‐6, CCL‐5 and leptin. These signals facilitate the recruitment of mast cells, lymphocytes and neutrophils around hair follicles, a consistent histopathologic finding of rosacea. ²⁷

MR studies in rosacea

MR has emerged as a crucial analytical tool for exploring causal relationships in rosacea. By using genetic variations as instrumental variables to examine the causal effect of exposures (such as lifestyle factors and metabolic variables) on the disease, MR minimizes biases from confounding and reverse causation seen in observational methods. ²⁸ , ²⁹ Recent MR analyses have highlighted smoking behaviour as a key factor: past smoking is associated with increased rosacea risk, whereas current smoking shows no significant link, pointing to complex exposure dynamics ³⁰ (Table 2). Alcohol intake shows variable associations, with some studies reporting increased rosacea risk in women with higher consumption. ²⁹ , ³¹ Furthermore, MR studies also support a bidirectional relationship between rosacea and inflammatory bowel disease (IBD), suggesting shared inflammatory mechanisms. ²⁸ , ³² Metabolic factors, such as blood metabolites, further implicate metabolic syndrome in rosacea. ²⁸ , ³³ Genetic susceptibility has been linked to polymorphisms in serotonin and adrenergic pathways, echoing patterns seen in other inflammatory conditions. ³⁴ , ³⁵

TABLE 2.

Gene–environment associations in rosacea: evidence from Mendelian randomization (MR) and exposome studies.

Exposure/factor	MR findings/epidemiological links	Associated pathways
Past smoking	Increased rosacea risk; current smoking shows no significant link	Oxidative stress, vascular dysregulation
Alcohol intake (high in women)	Variable association with increased risk	Vasodilation, neurovascular activation
IBD (Crohn's, UC)	Bidirectional association with rosacea	Shared inflammatory pathways (NOD2, HLA)
Metabolic syndrome/dyslipidaemia	Implicated in MR studies; epidemiological links with hypertension, insulin resistance	Endothelial dysfunction, systemic inflammation
Gut dysbiosis (SIBO)	Higher prevalence in rosacea; gut–skin axis role	Microbial metabolites, neuroimmune modulation
UV exposure	Genetic link and environmental trigger	TRP channel activation, ROS

Epidemiological studies have identified associations of rosacea with cardiometabolic comorbidities, including hypertension, dyslipidaemia and insulin resistance, as well as gastrointestinal dysbiosis, particularly small intestinal bacterial overgrowth (SIBO). The gut–skin axis may influence rosacea pathophysiology through microbial metabolites, systemic inflammation and neuroimmune modulation. ³⁶ , ³⁷ , ³⁸

INTRINSIC EXPOSOME

Rosacea's genetics and comorbid complexity

Genetic factors play a significant role in rosacea, with studies estimating that heritability accounts for 46% of the risk. Genetic predisposition is also linked to comorbidities such as cardiovascular disease, metabolic disorders and autoimmune conditions. Further associations are observed between rosacea and factors like age, BMI, exposure to UVR and skin cancer. ³⁹ Genome‐wide association studies (GWAS) have identified shared loci between rosacea and autoimmune diseases, particularly type 1 diabetes (T1D), celiac disease, multiple sclerosis and rheumatoid arthritis in females, with rheumatoid arthritis being the primary association in males. ⁴⁰ , ⁴¹

VEGF polymorphism (+405 C/G) is more prevalent in rosacea patients, with homozygous individuals exhibiting a higher risk. This suggests a role for VEGF in vascular dysregulation and angiogenesis, which are hallmarks of rosacea. ⁴² Rosacea might be linked to increased activity of reactive oxygen species (ROS) and impaired anti‐oxidant defenses. Glutathione S‐transferases (GSTs) play a key role in detoxifying ROS and electrophilic compounds. In rosacea, elevated GSTT1, GSTP1 and GSTM1 expression may result from GST activation due to excessive free radical generation by activated neutrophils or UV exposure. ⁴³ GSTT1 and/or GSTM1 null genotypes are associated with rosacea. ⁴⁴ These findings highlight the role of oxidative stress in rosacea pathogenesis (Table 1).

GWAS in Caucasians identified a single nucleotide polymorphism (SNP) rs763035, associated with rosacea, along with human leukocyte antigen (HLA) types HLA‐DRB1, HLA‐DQB1, and HLA‐DQA1, and IRF4, SLC45A2, and IL‐13 genes. ⁴⁰ , ⁴⁴ , ⁴⁵ These genetic markers are also associated with autoimmune conditions like T1D and celiac disease, reinforcing the inflammatory nature of rosacea. ⁴⁶ Additionally, a NOD2/CARD15 polymorphism R702W was identified in a patient with granulomatous rosacea and Crohn's disease ⁴⁷ and a BsmI polymorphism of the vitamin D receptor gene in patients with fulminant rosacea has been detected. ⁴⁸ Whole‐genome (WGS) and whole‐exome sequencing (WES) in Chinese families identified mutations in LRRC4, SH3PXD2A and SLC26A8, which are associated with increased vasoactive neuropeptide production, possibly contributing to neurogenic inflammation in rosacea ⁴⁹ (Figure 2 and Table 1).

FIGURE 2.

Rosacea pathogenesis: genetic, epigenetic and exposomal interactions. This figure illustrates the multifactorial pathogenesis of rosacea, integrating genetic predisposition, RNA‐based regulation, environmental exposures and clinical outcomes. Central inflammatory and vascular pathways—such as the TLR2–KLK5–LL‐37 axis, mast cell activation, TRPV channel signalling (TRPV1, TRPV4) and VEGF‐mediated angiogenesis—are modulated by genetic and epigenetic elements, as well as regulatory non‐coding RNAs (e.g. NEAT1, HOTAIR, ZNF667‐AS1) and micro‐RNAs. Exposomal triggers—including UV radiation, air pollution, heat, blue light, diet, alcohol, smoking, Demodex folliculorum, Helicobacter pylori, SIBO and stress—activate neurogenic inflammation via TRP channels and neuropeptides, promoting vasodilation and immune activation. Endothelial adhesion molecules (VCAM‐1, ICAM‐1 and E‐selectin), upregulated by UVB and inflammatory signals, contribute to leukocyte infiltration and sustained inflammation. Together, these pathways result in hallmark features of rosacea, including flushing, telangiectasia, papules/pustules and sebaceous gland hyperplasia, while also predisposing to systemic comorbidities like inflammatory bowel disease. This model emphasizes the value of exposome‐aware, personalized care strategies in rosacea management.

Non‐coding RNAs and biomarkers

Recent studies have explored the role of non‐coding RNAs (ncRNAs) in the pathogenesis of rosacea, providing new insights into the molecular mechanisms underlying the condition. RNA‐sequencing studies have identified long non‐coding RNAs (lncRNAs) and microRNAs (miRNAs) associated with immune cell migration and activation in rosacea subtypes, suggesting potential therapeutic targets (Table 3).

TABLE 3.

Non‐coding RNAs with possible regulatory role in rosacea.

Name	ncRNA type	Function/target
NEAT1	lncRNA	Promotes Inflammatory responses
HOTAIR	lncRNA	Inflammation suppressor
ZNF667‐AS1	lncRNA	Immune cell migration & activation
hsa‐miR‐1‐3p, hsa‐miR‐31‐5p, hsa‐miR‐21‐3p, hsa‐miR‐150‐5p, hsa‐miR‐223‐3p, hsa‐miR‐21‐5p, hsa‐miR‐424‐3p, hsa‐miR‐326, hsa‐miR‐342‐5p	miRNA	Upregulated Promote angiogenesis, inflammation (esp. in Papulopustular Rosacea (PPR))
hsa‐miR‐144‐3p, hsa‐miR‐199b‐5p, hsa‐miR‐451a, hsa‐miR‐149‐5p, hsa‐miR‐1246, hsa‐miR‐1290, hsa‐miR‐196a‐5p	miRNA	Downregulated Loss may enhance inflammatory and vascular signalling (esp. in PPR)

Key lncRNAs include NEAT1, which promotes inflammatory responses, HOTAIR, identified as an inflammation suppressor, and ZNF667‐AS1, which plays a role in immune cell migration and activation in rosacea. A total RNA‐sequencing study analysing samples from rosacea patients revealed 13 differentially expressed lncRNAs in the ETR subtype, 25 in the PhR, and 25 in the PPR. While subtype‐specific differences were observed, the majority of lncRNAs were linked to immune cell migration and/or activation. Computational bioinformatics analyses identified lncRNA‐miRNA interaction networks, with key lncRNAs acting as competing endogenous RNAs (ceRNAs) that regulate immune responses and T‐cell activation. Notably, NEAT1, HOTAIR and ZNF667‐AS1 acted as ceRNAs targeting hsa‐miR‐148b‐3p, hsa‐miR‐148a‐3p, hsa‐miR‐296‐3p, hsa‐miR‐378a and hsa‐miR‐152‐3p. ⁵⁰

In severe PPR patients, microRNA sequencing identified 16 differentially expressed miRNAs in the PPR lesional skin, many of which regulate angiogenesis and inflammation. ⁵¹ Specifically, 9 miRNAs were upregulated (hsa‐miR‐1‐3p, hsa‐miR‐31‐5p, hsa‐miR‐21‐3p, hsa‐miR‐150‐5p, hsa‐miR‐223‐3p, hsa‐miR‐21‐5p, hsa‐miR‐424‐3p, hsa‐miR‐326 and hsa‐miR‐342‐5p), whereas 7 miRNAs were significantly downregulated in the lesional skin of severe PPR (hsa‐miR‐144‐3p, hsa‐miR‐199b‐5p, hsa‐miR‐451a, hsa‐miR‐149‐5p, hsa‐miR‐1246, hsa‐miR‐1290 and hsa‐miR‐196a‐5p) compared to the non‐lesional skin.

Additionally, N6‐methyladenosine (m6A) RNA modifications have been linked to immune activity and may serve as biomarkers distinguishing molecular subtypes of rosacea. ⁵² Several potential biomarkers for rosacea have been suggested, including LL‐37, KLK5, TLR2, MMP‐9, cathelicidin, inflammasome proteins and neutrophil and macrophage markers. These biomarkers, primarily related to immune responses, could be useful not only in diagnosing rosacea but also in distinguishing its subtypes. ⁵³ Studies have shown that daily doxycycline treatment reduces KLK5, TLR2 and MMP‐9 levels, which correlated with clinical improvements. ⁵⁴ Advancements in biomarker research have improved our understanding of rosacea and may aid in diagnosis and treatment (Figure 2).

Rosacea in skin of colour

Traditionally linked to fair skin, rosacea remains underdiagnosed in individuals with skin of colour (SOC). While prevalence rates are significantly higher in lighter‐skinned populations compared to African nations, ⁵⁵ this disparity may not accurately reflect the actual incidence in darker‐skinned individuals due to limited awareness and diagnostic challenges. ⁵⁶ , ⁵⁷ Symptoms such as erythema and telangiectasia can be subtle or misinterpreted in darker tones, further delaying diagnosis. ⁵⁸ The clinical features of rosacea are heterogeneous and can significantly affect quality of life (QoL), emphasizing the need for tailored diagnostic approaches. ⁵⁹ Clinician bias and the historical association of rosacea with lighter skin exacerbate this issue. ⁵⁷

Management in SOC requires special considerations. Laser therapies carry a higher risk of hypopigmentation and scarring due to increased melanin content. ⁵⁹ Additionally, the impaired skin barrier function in rosacea necessitates careful selection of topical treatments. ⁶⁰

Greater awareness and education are essential in improving rosacea recognition and management in SOC. Expanding research on rosacea pathogenesis, microbiota and tailored treatment protocols will improve care outcomes. ²³ , ⁶¹ , ⁶² Addressing these disparities ensures better QoL and care for all affected individuals (Figure 1).

Cutaneous microbiome and gut axis

The microbiome, both on the skin and in the gut, is implicated in rosacea pathogenesis. Rosacea patients have a higher prevalence of Demodex mites, particularly Demodex folliculorum, compared to healthy individuals. These mites promote inflammation by stimulating Toll‐like receptor 2 (TLR2), increasing LL‐37, which leads to angiogenesis. Systemic increase of IL‐8 and TNF‐α, also possessing angiogenic properties, has also been observed in patients with increased Demodex densities. ⁶³ Increased vascular endothelial growth factor (VEGF) in rosacea skin is thought to suppress local immunity, encouraging Demodex proliferation and contributing to low‐level inflammation and T‐cell exhaustion. ⁶⁴ They are found in higher densities in ETR and PPR subtypes. ⁶⁵ , ⁶⁶ , ⁶⁷

Meantime, Demodex mites may carry Bacillus oleronius, a bacterium associated with rosacea. ⁶⁸ Additionally, Staphylococcus epidermidis, a common skin commensal, is found in a beta‐hemolytic, possibly more virulent form in rosacea pustules. Interestingly, Cutibacterium acnes in PPR were more similar to that of acne pustules than to that of rosacea without inflammatory papules and pustules. ⁶⁹ This suggests that both anti‐inflammatory and antibacterial mechanisms may underlie the efficacy of certain treatments for rosacea.

MR using SNPs from GWAS analyses suggests causal links between skin microbiome variations and acne/rosacea. Acne is associated with bacterial genera including Corynebacterium, Bacilli, Staphylococcus and Bacteroides. In rosacea, an uncategorized Staphylococcus ASV is linked with increased risk ⁷⁰ (Figure 1).

Gut microbiome

The gut–skin axis plays a significant role in rosacea, particularly via microbial dysbiosis and systemic inflammation. Among gut microbiome disturbances, SIBO and Helicobacter pylori infection are the most frequently reported in rosacea patients. H. pylori may contribute to the ETR subtype by releasing nitric oxide, gastrin and TNF‐α, which promote vasodilation, angiogenesis and flushing. ⁷¹ While studies suggest an association between SIBO and rosacea, findings are inconsistent, and causality remains unclear. ³⁸ , ⁷² , ⁷³ Notably, SIBO appears more consistently associated with the PPR subtype, and some trials report remission of rosacea after SIBO eradication with rifaximin or antibacterial botanical supplementation. ⁷⁴ , ⁷⁵

Beyond microbial imbalance, IBD has been linked to a higher risk of rosacea, though MRS data suggest the association may be unidirectional, meaning IBD increases rosacea risk but not vice versa. ⁷⁶ Specifically, rosacea is associated with a greater risk of Crohn's disease (CD), and tetracycline therapy—commonly used for rosacea—has been linked to an elevated risk of both CD and ulcerative colitis (UC). ⁷⁷ , ⁷⁸ Additionally, celiac disease has also been observed more frequently in rosacea patients, reinforcing the role of systemic and autoimmune mechanisms in rosacea pathogenesis ⁷⁹ (Figure 2).

Hormonal factors in rosacea

Rosacea has been associated with increased topical steroidogenesis, with increased cortisol production in the skin contributing to the disease pathogenesis. This mechanism may mediate environmental triggers, such as UVB exposure, which also increases skin steroidogenesis. Supporting this is the observation that chronic topical steroid use can cause steroid‐induced rosacea‐like dermatitis, a condition resembling rosacea. ⁸⁰ Corticotropin‐releasing hormone (CRH) is another key factor, driving pro‐inflammatory cytokine production and vasodilation, potentially explaining stress‐induced rosacea exacerbations. ⁸¹ , ⁸² In addition, UVB influences skin CRH production, reinforcing the connection between UVB exposure, skin steroidogenesis and rosacea. ⁸³

The protective role of oestrogens in skin health has often been suggested as well as the likely susceptibility of perimenopausal women to several dermatoses. ⁸⁴ Oestrogen's anti‐inflammatory and vascular‐stabilizing effects may help alleviate rosacea symptoms. ⁸⁵ Conversely, progesterone has been associated with vasodilation and skin sensitivity, possibly exacerbating the condition. Oestrogen‐containing contraceptives may benefit some women, whereas progestin‐only contraceptives, such as some hormonal intrauterine devices (IUDs), might exacerbate symptoms. These IUDs release synthetic progestin (levonorgestrel), which has androgenic effects and theoretically contributes to flushing, increased sebum production and inflammation. Along these lines, perimenopausal women with ETR exhibit a more severe phenotype; the greater the reduction in the serum estradiol levels. ⁸⁶

Clinical evidence suggests that hormonal IUDs increase rosacea flare, compared to oral contraceptives. ⁸⁷ , ⁸⁸ In a 5‐year follow‐up study, the use of hormonal intrauterine devices has been associated with increased rosacea incidence compared to non‐hormonal intrauterine devices. While copper IUDs do not release hormones, they may still provoke inflammatory responses due to increased prostaglandins, which could theoretically trigger or exacerbate rosacea flares. The levonorgestrel release rate may influence rosacea severity, but the risk is generally not severe enough to necessitate discontinuation (Figure 2).

Obesity and metabolic syndrome

Studies show associations between rosacea, obesity and weight gain, possibly categorizing high BMI as a risk factor. Although the underlying mechanism has not been clearly elucidated, the low‐grade inflammation present in the obese state is likely to be involved. ⁸⁹ , ⁹⁰ Interestingly, obese rosacea patients tend to have more severe manifestations of the disease and are more likely to display demodex infestation than non‐obese patients. ⁹¹ This may show a link between obesity and demodicosis in rosacea pathogenesis. Additionally, increased skeletal muscle mass has been shown to have a protective effect on severe ETR and PPR, although not on mild cases. ⁹² On the contrary, in a study on the association of obesity and spicy‐food consumption with rosacea, obesity was not found to be a risk factor; rather, underweight was associated with rosacea risk. Moderate spicy food consumption alleviated that risk and was also protective among the obese group. ⁹³ Additionally, adherence to a Mediterranean‐like dietary pattern could reduce the risk of rosacea in non‐obese individuals. ⁹⁴

Insulin resistance is more prevalent among rosacea patients. In the same study, although rosacea showed no correlations with metabolic syndrome, it was associated with higher fasting blood glucose, cholesterol levels and arterial pressure. Family history of cardiovascular disease was also more common in rosacea patients compared to normal controls. ⁹⁵ These results were supported in two systematic meta‐analyses ⁹⁶ , ⁹⁷ (Figure 1).

Psychosocial burden and mental health in rosacea care

Rosacea's visible symptoms often lead to psychosocial distress, including anxiety, depression and social withdrawal. Patients with rosacea experience higher rates of depression and reduced quality of life compared to the general population. ⁹⁸ , ⁹⁹ , ¹⁰⁰ Additionally, the frequent misperception of rosacea‐related facial erythema as alcohol‐related adds to social stigma and emotional discomfort. ⁹⁹ In a survey, 62% of respondents reported work and social life impairment, while 26.1% actively avoided social interactions. ¹⁰¹

Psychological factors, particularly anxiety, depression and decreased quality of life, are emerging as important factors in rosacea. ¹⁰⁰ , ¹⁰² , ¹⁰³ , ¹⁰⁴ , ¹⁰⁵ Sleep disturbances are also increasingly recognized in rosacea. Poor sleep quality and deprivation are linked to more severe disease phenotypes. ¹⁰⁶ Animal studies suggest that sleep deprivation may exacerbate inflammation by upregulating LL‐37, TLR‐2 and VEGF expression. ¹⁰⁷ Importantly, effective treatment and improvement of rosacea symptoms have been associated with improved mental health, including reduced anxiety, improved sleep and quality of life. ¹⁰⁸ Given these associations, psychological counselling, mental health support, alongside dermatologic care should be integrated into rosacea management to address its psychological burden effectively (Figures 1 and 2).

EXTRINSIC EXPOSOME

Environmental exposome and UVR in rosacea

Ultraviolet radiation

As detailed in the pathophysiology section, UVR amplifies inflammatory and vascular cascades in rosacea. Clinically, patients with the ETR subtype are particularly sensitive. Chronic UV exposure, temperature fluctuations and airborne pollutants correlate with severity and flares. ¹⁰⁹ UVB radiation promotes vascular inflammation by upregulating adhesion molecules, such as VCAM, ICAM and E‐selectin, while directly damaging keratinocytes (Figures 1 and 2). This cellular damage leads to the release of dsRNA and increased LL‐37 expression, both of which enhance leukocyte infiltration and activate inflammatory cascades that exacerbate rosacea. ¹¹⁰ Demodex mites, which are more prevalent in rosacea patients, contribute to inflammation by stimulating TLR2 and further increasing LL‐37. This process creates a vicious cycle, where mite proliferation enhances skin sensitivity to UVB, which in turn amplifies immune responses, increases VEGF expression and exacerbates both ETR and PPR subtypes. ¹¹⁰ , ¹¹¹ , ¹¹²

Sun exposure has been positively correlated with symptom severity in the ETR subtype, while its role in other subtypes remains variable. ¹¹³ Notably, non‐facial UV exposure plays a minor role in symptom exacerbation, highlighting the localized impact of solar radiation on facial skin. Preventive photoprotection remains a cornerstone of rosacea management. Broad‐spectrum sunscreens with physical blockers such as zinc oxide and titanium dioxide are recommended for UV‐induced flares. ¹¹⁴

Blue light from electronic devices

In recent years, growing attention has been given to the impact of visible light, particularly blue light (wavelength 400–490 nm), on inflammatory skin disorders. Blue light is a component of both natural sunlight and artificial sources such as LED lighting, smartphone screens, tablets and computer monitors. For individuals with rosacea, exposure to blue light may represent a significant, underrecognized environmental trigger ¹¹⁵ , ¹¹⁶ (Figure 1).

Blue light penetrates the skin and generates reactive oxygen species (ROS), which trigger inflammation and may worsen rosacea symptoms. It may impair the skin barrier, increasing water loss and sensitivity to triggers. ¹¹⁵ , ¹¹⁷ , ¹¹⁸ It can activate neuropeptides and exacerbate neurogenic inflammation, contributing to flushing and burning. Meantime, there is speculation that blue light could affect Demodex and microbiome balance, factors relevant in rosacea. ¹¹⁹ Therefore, patients with rosacea should consider reducing screen time, using blue light filters or night mode, and applying topical antioxidants (e.g. niacinamide, vitamin C) ¹²⁰ (Figure 2).

Environmental conditions and airborne pollutants

Climate change effects, temperatures both extreme heat and cold, have been shown to exacerbate rosacea symptoms. ¹²¹ Heat induces vasodilation and increases blood flow, triggering flushing and erythema, whereas cold temperatures and wind promote vasoconstriction, irritation and inflammatory mediator release. ¹²² , ¹²³ , ¹²⁴ Humidity levels and wind exposure further contribute to symptom variability, reflecting the complexity of the environmental exposome's role in disease severity. ¹²⁵

Air pollutants such as particulate matter (PM2.5), nitrogen dioxide (NO₂) and ozone are emerging as significant triggers in inflammatory skin diseases and rosacea. ⁷ These pollutants contribute to oxidative stress, disrupt the skin barrier and activate inflammatory signalling pathways. Urban living, often burdened by elevated pollutant levels, demonstrates a higher prevalence of rosacea, underscoring the need to recognize pollution as a major and underappreciated environmental risk factor. ¹²⁶

Occupational environmental exposure

Individuals employed in outdoor or industrial settings face compounded risk due to prolonged UV exposure and contact with environmental irritants. Outdoor workers, such as farmers and construction personnel, are particularly vulnerable, as cumulative lifetime sun exposure significantly contributes to the development and exacerbation of rosacea. ³⁹ , ⁸² , ¹²⁷ , ¹²⁸ Furthermore, occupational exposure to chemical irritants, including solvents, cleaning agents, industrial dusts and fumes, can act as physical or chemical triggers for rosacea flares. ¹²⁹ Workers in construction, manufacturing and agriculture are especially at risk due to the synergistic impact of UV and environmental pollutants.

During the COVID‐19 pandemic, the use of personal protective equipment (PPE) such as goggles and face shields became widespread, particularly in industrial and healthcare settings. These facial PPEs have been associated with exacerbation of pre‐existing facial dermatosis, such as rosacea and acne. ¹³⁰ , ¹³¹ , ¹³² , ¹³³

Heat triggers

Heat exposure from environmental conditions or activities that raise body temperature is another well‐documented trigger for rosacea, especially ETR and PPR. ¹³⁴ Heat‐induced vasodilation can lead to prolonged facial erythema in patients with ETR and PPR subtypes. Notably, women exposed to high temperatures from traditional ovens (e.g., tandoor cooking) have demonstrated a higher prevalence of rosacea. ¹³⁵

Daily activities, such as hot baths, intense exercise and the consumption of hot beverages, are common triggers. Studies indicate that the temperature of beverages, rather than the caffeine content, is the primary exacerbating factor. ¹³⁶ Interestingly, coffee consumption has been associated with a reduced risk of rosacea, likely due to its vasoconstrictive and anti‐inflammatory properties. ¹³⁷

Diet and lifestyle

Nutrition

Dietary factors significantly influence rosacea, with certain foods and beverages identified as common triggers. Alcohol, spicy foods, fried foods, refined sugars, chocolate, dairy and certain fruits like citrus are frequently reported as triggers. Cinnamaldehyde, found in cinnamon, tomatoes, chocolate and citrus fruits, activates sensory nerve receptors, leading to inflammation and symptom exacerbation. Capsaicin, present in spicy foods, similarly activates TRP channels, particularly TRPA1 and TRPV1, which are also triggered by UV radiation and alcohol. ¹³⁸

Emerging evidence suggests that anti‐inflammatory dietary patterns, such as the Mediterranean diet, rich in vegetables, nuts, whole grains, tea and omega‐3 fatty acids, may have a beneficial effect on rosacea. ⁹⁴

A high intake of fatty foods has been linked to increased rosacea risk, potentially due to inflammation and epidermal barrier disruptions in ceramide and hyaluronic acid homeostasis. ⁹⁴ , ¹³⁹ , ¹⁴⁰ Interestingly, frequent dairy consumption appears to have a protective effect, though further studies are needed. ¹⁴¹ While these dietary changes have been more extensively studied in acne, similar mechanisms may apply to rosacea patients. ¹³⁷ However, dietary counseling is not routinely integrated into rosacea management.

Alcohol consumption

The relationship between alcohol consumption and rosacea is complex, with both positive and neutral findings across studies. ¹⁴⁰ Alcohol consumption has been associated with the PhR subtype and not with other rosacea subtypes. ¹⁴² A proposed mechanism for alcohol‐induced flares is histamine intolerance, particularly in response to histamine‐rich foods and beverages such as red wine and liquors. Acetaldehyde and acetone, metabolic by‐products of alcohol, may contribute to flushing and inflammation. ¹³⁸

A large cohort study found that alcohol intake, particularly white wine and liquor, increased rosacea risk, with higher alcohol intake correlating with higher disease severity. ¹⁴³ However, other studies have found no significant differences in alcohol consumption between rosacea patients and healthy controls, suggesting that individual susceptibility factors play a role. ⁷³

Smoking

The impact of smoking on rosacea is debated, with studies offering contradictory findings. Smoking is more prevalent among rosacea patients, particularly those with the ETR subtype. This may be due to the angiogenic effects of nicotine counteracting its anti‐inflammatory properties. ¹⁴⁴ Another study suggests that ex‐smokers are more likely to develop rosacea than active smokers, indicating a possible protective effect of nicotine that diminishes after cessation. ⁷³ , ¹⁴⁵

Skincare practices and cosmetic use

Rosacea patients often follow distinct facial skincare routines that may influence symptom severity. They are less likely to use cleansers and makeup, often relying on water alone for facial cleansing, and more likely to take hot baths, which can exacerbate symptoms. ⁶⁸

A study on Chinese adolescents identified frequent use of facial cleansers (≥2 times daily) and prolonged bath duration as risk factors for rosacea, while water temperature and bath frequency showed no correlation. Notably, sun protection did not seem to exert any protective effect in this study. ¹⁴⁶

Similarly, a large study on Chinese adolescents found that foaming cleansers, frequent makeup use (>6 times weekly), facial masks (>4 times weekly) and beauty salon facial treatments (>1 time weekly) were correlated with rosacea, while moisturizing products, sunscreen and moderate cleansing (1–3 times weekly) were beneficial. ¹⁴⁷

Aggressive skincare habits including deep cleansing, frequent exfoliation and overuse of face masks exacerbate rosacea by worsening symptoms and expanding affected areas. ¹⁴⁸ A history of allergic reactions to skincare products further increases rosacea risk, with the frequency of the reactions correlating to higher susceptibility. ¹⁴⁹ Ingredients like alcohol and other dehydrating agents should be avoided. ¹⁵⁰ Given the key role of UVB in rosacea pathogenesis, sun protection is an integral part of rosacea management. ⁸² High‐protection sunscreen effectively reduces erythema, dryness and scaling. ¹⁵¹ Proper skincare should prioritize skin barrier integrity, hydration and pH balance. Usage of gentle, soap‐free cleansers with a near‐physiological pH (4–7), fragrance‐free, ceramide‐ and niacinamide‐containing moisturizers, and daily sunscreen of an SPF ≥30 is highly recommended. ¹⁵² , ¹⁵³ , ¹⁵⁴ These recommendations extend to SOC patients, although data on their effectiveness in this population is limited. ¹⁵⁵

Rosacea and social determinants of health

Social determinants of health (SDOH), including socio‐economic status (SES), environmental exposures, healthcare access, education and social support, profoundly impact the prevalence, severity and management of rosacea. Individuals with lower SES often face barriers in accessing dermatologic care, leading to delayed diagnoses and suboptimal treatment, which can negatively affect disease trajectory. ¹⁵⁶ , ¹⁵⁷ Additionally, high out‐of‐pocket costs for prescription medications, laser therapy and specialized dermatologic care further exacerbate disparities. ¹⁵⁸

Underdiagnosis of rosacea in individuals with darker skin tones (Fitzpatrick IV–VI) remains a significant concern, partly due to limited representation in clinical trials and difficulty detecting erythema. ¹⁵⁹ Environmental triggers, such as UVR, air pollution and extreme temperatures, vary by region. Urban populations may experience higher pollution levels, whereas rural populations may have greater occupational sun exposure. ¹⁵⁹

Limited healthcare access further contributes to disparities in rosacea care. Patients without insurance may rely on primary care providers with limited expertise in rosacea management. ¹⁶⁰ Moreover, rural and underserved communities often lack dermatologists, leading to delayed diagnosis and treatment. Teledermatology emerged as a valuable tool for improving access, particularly in underserved areas. ¹⁶¹

Addressing these issues requires a multifaceted approach, including educating primary care providers on rosacea recognition and management, expanding access to specialized dermatologic care in underserved areas, and integrating psychosocial screening and counselling into rosacea management. Additionally, treatment plans should consider SDOH to ensure the affordability and accessibility of effective therapies. ¹⁶⁰ By tackling these disparities, patients with rosacea will improve their QoL, regardless of skin type or socio‐economic background.

Rosacea disinformation and misinformation in social media

Disinformation about rosacea on social media poses significant challenges for both patients and healthcare providers. Dermatologists must be aware of widespread misinformation across platforms, including harmful conspiracy theories and inaccurate medical advice that exploit patients' psychological vulnerability. ¹⁶² , ¹⁶³ Moreover, individuals with moderate to severe rosacea, particularly those lacking proper care, are highly susceptible to misinformation, which exacerbates anxiety, depression as well as the psychosocial burden, including low self‐esteem and social withdrawal. ¹⁶² , ¹⁶⁴ Misinformation spreads rapidly on social media due to systemic biases favouring provocative content, and removed posts often reappear in different formats, perpetuating the cycle. As social media remains a key health information source, healthcare professionals must actively promote credible resources and educate patients on the risks of unreliable content. ¹⁵⁰ Addressing rosacea‐related disinformation requires a concerted effort to counteract misleading narratives and support better patient outcomes.

EXPOSOMAL RELEVANCE OF ROSACEA THERAPY

Rosacea treatment requires a multifaceted approach tailored to clinical subtype, severity and underlying exposomal factors (Table 4 and Figure 3). Classical therapies remain foundational, including topical agents such as metronidazole, azelaic acid, ivermectin and brimonidine for erythema and inflammation, and oral tetracyclines like doxycycline for papulopustular flares due to their anti‐inflammatory properties.  ⁹ , ⁵⁴ , ¹⁰⁶ , ¹⁶⁵ , ¹⁶⁶ , ¹⁶⁷ , ¹⁶⁸ , ¹⁶⁹ , ¹⁷⁰ , ¹⁷¹ , ¹⁷² , ¹⁷³ , ¹⁷⁴ , ¹⁷⁵ , ¹⁷⁶ , ¹⁷⁷ , ¹⁷⁸ Laser and light therapies (e.g. pulsed dye laser, intense pulsed light) are effective for telangiectasia and persistent erythema, though caution is warranted in patients with skin of colour due to pigmentary risks ² , ⁹ , ⁵⁹ , ¹⁰⁹ , ¹⁶⁵ , ¹⁷⁸ , ¹⁷⁹ , ¹⁸⁰ , ¹⁸¹ , ¹⁸² , ¹⁸³ (Table 4).

TABLE 4.

Exposome‐informed therapeutic strategies for rosacea management.

Therapeutic category	Agents/modalities	Mechanism of action	Exposome interaction	References
Topical agents	Metronidazole, Azelaic acid, Ivermectin	Anti‐inflammatory, anti‐parasitic	Efficacy may decline with environmental pollutants UV exposure increases oxidative stress	[9, 106, 165, 166, 167, 168, 169, 170, 171, 172, 173]
Systemic antibiotics	Doxycycline (subantimicrobial dose)	Anti‐inflammatory, MMP inhibition	Reduced efficacy in smokers. UV may exacerbate inflammation during treatment	[9, 54, 174, 175]
Topical vasoconstrictors	Brimonidine, Oxymetazoline	α‐adrenergic agonists; transient vasoconstriction	Vasodilation due to heat, alcohol or stress can override effects	[176, 177, 178]
Laser & Light therapies	Pulsed dye laser, intense pulsed light (IPL)	Photothermolysis of superficial vessels	Post‐treatment care must consider UV/pollution. Darker skin tones risk hyperpigmentation	[59, 109, 182, 183]
Isotretinoin (off‐label)	Low‐dose oral isotretinoin	Sebaceous gland suppression, anti‐inflammatory.	Environmental factors (e.g. dry air, UV) can exacerbate irritation.	[191, 192, 193, 194, 195, 196]
Lifestyle and barrier care	Gentle cleansers, moisturizers, sunscreen	Barrier repair, photoprotection	Essential in mitigating damage from UV, heat, cold, pollutants	[154, 170, 186]
Topical anti‐oxidants	Vitamin C, niacinamide	Reduce ROS, soothe inflammation	Target pollution‐ and blue light‐induced oxidative stress	[82, 187, 188]
Dietary modulation	Anti‐inflammatory diet, histamine avoidance	Reduces inflammation, modulates gut–skin axis	Diet‐related triggers like alcohol and spicy foods, activate TRP channels	[94, 139, 140]
Probiotics/microbiome	Topical or oral (emerging)	Rebalancing microbial dysbiosis	Gut and skin microbiome disrupted by antibiotics, pollutants, poor diet	[140, 188, 189, 190]
Anti‐parasitic therapy	Ivermectin	Targets Demodex mites and reduces inflammation	High Demodex density is linked with UV exposure and barrier dysfunction.	[168, 170, 172, 173, 197]
Hormonal modulation	Oral contraceptives, oestrogen therapy	Modulates vasodilation and inflammation, stabilizes skin barrier	Perimenopause, hormonal IUDs and low oestrogen exacerbate symptoms.	[88, 106]
Anti‐SIBO treatment	Rifaximin, herbal antimicrobials	Eradicates small intestinal bacterial overgrowth, reduces systemic inflammation.	Gut–skin axis: SIBO linked to persistent papulopustular rosacea.	[38, 74, 75, 140]

FIGURE 3.

Exposome relevant rosacea therapies.

Informed by emerging molecular and exposomal insights, newer interventions target the microbiome, immune dysregulation and barrier dysfunction. ¹⁸⁴ , ¹⁸⁵ These include barrier‐repairing moisturizers with ceramides and niacinamide, and topical antioxidants like vitamin C to counteract UV‐ and pollution‐induced oxidative stress. ⁸² , ¹⁵⁴ , ¹⁷⁰ , ¹⁸⁶ , ¹⁸⁷ , ¹⁸⁸ Emerging therapies such as probiotics are under investigation. ¹⁴⁰ , ¹⁸⁸ , ¹⁸⁹ , ¹⁹⁰ In addition, administration of low‐dose oral isotretinoin has also been suggested, especially for non‐responders to classical regimens. ¹⁹¹ , ¹⁹² , ¹⁹³ , ¹⁹⁴ , ¹⁹⁵ , ¹⁹⁶ For Demodex‐associated rosacea, topical acaricides such as permethrin and oral ivermectin may be beneficial. ¹⁶⁸ , ¹⁷⁰ , ¹⁷² , ¹⁷³ , ¹⁹⁷ In hormone‐sensitive cases, especially perimenopausal women, hormone modulation may influence symptom control ⁸⁸ , ¹⁰⁶ (Table 4). Future directions include targeted therapies against TLR2, KLK5 and TRP channels and biologic agents under investigation for severe or refractory cases ¹⁸⁸ (Figure 3).

Ultimately, integrating exposome‐aware lifestyle modifications, like UV protection, dietary adjustments, heat avoidance and psychological support, enhances therapeutic efficacy and patient quality of life. ³⁷ , ¹³⁹ , ¹⁴⁰

CONCLUSIONS

Rosacea is more than just a dermatologic condition; it is a complex disorder shaped by a dynamic interplay of genetic predisposition, immune dysregulation, environmental exposures and lifestyle factors. The increasing recognition of the exposome's role in rosacea pathogenesis underscores the need for a comprehensive, patient‐centred approach that extends beyond conventional dermatologic treatments. Addressing modifiable exposomal factors, such as UV exposure, diet and microbiome health, can improve disease outcomes and QoL. Strategies such as personalized skincare, dietary modifications, microbiome‐targeted therapies, and addressing psychosocial burdens can improve patient outcomes. Furthermore, disparities in diagnosis and management, particularly among SOC populations, highlight the need for greater awareness and inclusive research. Additionally, there should be support for insurance policies that include coverage for dermatological conditions and advanced treatments for rosacea.

The increasing global burden of climate change, characterized by rising temperatures, worsening air pollution and extreme weather events, is anticipated to further impact the incidence and severity of rosacea. The promotion of policies that support sun protection measures (e.g. UV‐protective clothing, access to sunscreen) in high‐risk occupations should be promoted. Importantly, the fight against stigma through educational initiatives that increase understanding of rosacea and its non‐contagious nature is important. Finally, reducing air pollution and improving urban planning to minimize environmental exposures that contribute both to the sustainability of skin health overall and to the outbreak of rosacea.

Future investigations should focus on elucidating molecular pathways, refining targeted therapies and integrating exposome‐based interventions into clinical practice. More specifically, research approached on rosacea should be revisited through the current advancements in methodologies and multi‐omics approaches integrating genomic, epigenetic, transcriptomic, microbiome and exposome data to define molecular signatures for precision medicine. Such patterns could address diagnostic gaps through multiethnic cohort studies and inclusive phenotyping in skin of colour. Longitudinal exposome monitoring would help unravel trigger–flare dynamics, while elucidation of novel pathways involving TRP channels, neurogenic inflammation, adhesion molecules and non‐coding RNAs is important and, so far, essentially underexplored. Finally, prevention‐oriented interventional trials that combine lifestyle, dietary, psychosocial and pharmacologic strategies, supported by algorithm‐based tools for clinicians, could shift care towards precision and prevention‐focused care. Undoubtedly, a deeper understanding of these factors will pave the way for more effective prevention and treatment strategies, improving both outcomes and QoL for individuals affected by rosacea.

AUTHOR CONTRIBUTIONS

K.G., D.B.S., A.M. and E.P. contributed to the manuscript writing and figure design and approved the review for publication. All authors have read and agreed to the published version of the manuscript.

FUNDING INFORMATION

None.

CONFLICT OF INTEREST STATEMENT

None declared.

ETHICAL APPROVAL

Ethical approval was not required, since the paper did not involve research with human participants.

ETHICS STATEMENT

Not applicable.

Grafanaki K, Bakoli Sgourou D, Maniatis A, Pasmatzi E. The exposomal imprint on rosacea: More than skin deep. J Eur Acad Dermatol Venereol. 2026;40:387–403. 10.1111/jdv.70112

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available from the corresponding author upon reasonable request.