Inflammation in cardio-oncology and psychological disorders: mechanisms, biomarkers, pain management, and therapeutic strategies

Abstract

Chronic inflammation is the key pathophysiological link between psychological disorders and cardio-oncology, two seemingly separate clinical domains with increasingly acknowledged interdependencies. The inflammatory cascade not only plays a role in the etiology and development of several psychological disorders but is also a common biological substrate for cardiovascular difficulties in cancer patients (cardio-oncology). Despite mounting evidence of this tripartite link, clinical practice still uses fragmented integrated approaches to treating these interrelated illnesses. The purpose of this review is to compile the most recent data regarding the inflammatory pathways that are common to psychological illnesses, oncological processes, and cardiovascular side effects of cancer treatment. We examine how psychological discomfort in cancer patients worsens cardiovascular outcomes and how cardiovascular problems affect psychological well-being oppositely. Additionally, we assess new inflammatory biomarkers that may be useful for both diagnosis and prognosis in these disorders. This review offers a thorough framework for clinicians and researchers to address the intricate relationships between cancer treatment, psychological functioning, and cardiovascular health. It does so by looking at the most recent developments in anti-inflammatory interventions, pain management techniques, and integrated therapeutic approaches. Our goal is to draw attention to potential targeted therapies that use inflammatory pathway regulation to address several facets of this clinical triad at once.

HIGHLIGHTS

• Inflammation as a key driver of cardiotoxicity: Cancer therapies, including chemotherapy, radiotherapy, and Chimeric Antigen Receptor T cell therapy, induce cardiotoxicity by activating inflammatory pathways, leading to myocardial damage and cardiovascular disease.

• Chronic inflammation in cancer patients: Persistent inflammation in cancer patients exacerbates cardiovascular risks, contributing to endothelial dysfunction, atherosclerosis, and heart failure.

• Stress-inflammation link: Chronic stress triggers inflammatory responses via hypothalamic-pituitary-adrenal axis dysregulation, increasing the risk of cardiovascular diseases and psychological disorders such as depression.

• Biomarkers for early detection: C-reactive protein, Interleukin-6 (IL-6), and Tumor Necrosis Factor alpha (TNF-α) serve as key biomarkers for predicting cardiotoxicity and psychological distress in cancer patients, enabling early risk stratification.

• Pain management and inflammation: Perioperative pain management strategies, including opioids, non-steroidal anti-inflammatory drug (NSAIDs), and regional anesthesia, influence inflammatory responses and cardiovascular outcomes in cancer patients.

• Integrating psychological support: Addressing psychological distress in cancer patients through mindfulness, behavioral interventions, and pain control improves cardiovascular and mental health outcomes.

• Therapeutic strategies: Pharmacological approaches (NSAIDs, immunomodulators) and non-pharmacological interventions (lifestyle changes, traditional Chinese medicine) can help modulate inflammation and reduce cardiovascular risk.

Introduction

In the evolving field of cardio-oncology, the intersection of cardiovascular health and cancer treatment has revealed inflammation as a common link driving both cardiotoxicity, tumor progression, and psychological disorders^[1–3].

The proinflammatory environment shared by cancer and cardiovascular disease (CVD) likely plays a key role in their development and mutual exacerbation. Furthermore, chemotherapy improves cancer survival but is also associated with cardiotoxicity and inflammation. This inflammation may worsen CVD through mechanisms that are not yet fully understood^[4]. It induces tumor cell death by triggering the release of growth factors, cytokines, and damage-associated molecular pattern (DAMPs), fostering inflammation and therapy resistance. This unintended consequence critically influences therapeutic response and relapse likelihood^[5].

Growing evidence shows links between mental stress, oxidative stress, and systemic inflammation to psychological disorders like depression, anxiety, and cognitive impairment, driven by complex inflammatory mechanisms^[3]. Conversely, acute and chronic psychological stress can trigger inflammation through increased sympathetic output and cytokine release, exacerbating CVD risk^[6]. This interplay highlights the need to explore inflammation as a unifying factor in cardio-oncology and psychological disorders, offering new insights into their interconnected pathophysiology.

In cancer, inflammation drives tumorigenesis by inducing DNA damage and oxidative stress^[5], while cell death promotes cytokine release, leading to pro-tumor inflammation, treatment resistance, and related cardiotoxicity, which worsen cardiovascular complications^[7]. Similarly, it plays a role in mental stress and psychological disorders (depression, anxiety, and cognitive impairment), exacerbating these conditions^[3].

Understanding inflammation’s mechanisms and identifying biomarkers are vital for early detection, personalized treatments, and effective pain management, ultimately improving outcomes for patients with cancer, enhancing quality of life (QOL) for cancer survivors with chronic pain, and addressing psychological disorders. In pain management, opioids are commonly used for moderate to severe cancer pain^[8]. They also modulate inflammatory pathways and are associated with significant side effects, underscoring the need for balanced, comprehensive therapeutic strategies.

This review aims to bridge the knowledge gap by examining mechanisms, biomarkers, and therapeutic strategies. It seeks to comprehensively understand inflammation as a shared link and explore multifactorial interventions to mitigate its detrimental effects across these interconnected fields.

Mechanisms linking inflammation, cardio-oncology, and psychological disorders

Inflammatory mechanisms in cancer therapy-induced cardiotoxicity

Cancer therapies, including chemotherapy, radiotherapy, and targeted therapies, can lead to cardiovascular toxicity, with inflammation playing a critical role in this process.

Anthracyclines induce cardiotoxicity primarily through excessive reactive oxygen species (ROS) production, lipid peroxidation, and mitochondrial damage. ROS activates the NLRP3 inflammasome, triggering pro-inflammatory cytokine release and pyroptosis, which recruits leukocytes to the myocardium, exacerbating tissue damage and inflammation^[9]. According to a recent report, >50% of patients experience subclinical pathological alterations in left ventricular function, such as elevated afterload or impaired systolic function, within 1 year following anthracycline therapy^[10].

Immune checkpoints inhibit T cell-mediated autoimmune activation in myocardium, and their inhibition may lead to local T cell activation, causing cross-reaction with myocardial antigens and cardiac dysfunction^[9,11]. In Chimeric Antigen Receptor T (CAR-T) cell therapy, the CAR-T cells induce pyroptosis, releasing DAMPs that activate macrophages. These macrophages initiate a cycle of immune activation and cytokine release, further exacerbating cardiotoxicity^[12]. Radiotherapy leads to DNA damage and the production of ROS. This triggers inflammation, leading to endothelial damage, thereby promoting atherosclerosis, increasing the risk of coronary artery disease and heart failure^[13]. Amongst breast cancer patients receiving radiotherapy, particularly left-sided, a dose-dependent increase in the risk of developing ischemic heart disease has been reported^[10].

These findings suggest inflammation is a key mechanism underlying cardiotoxicity and highlight the need for strategies targeting inflammation to mitigate cardiotoxicity in cancer survivors. Building upon the understanding of how inflammation contributes to direct cardiac damage during cancer treatment, it is crucial to also consider the broader impact of chronic inflammatory processes on the long-term cardiovascular health of cancer patients, extending beyond the immediate effects of therapy.

Role of chronic inflammation in cardiovascular risk among cancer patients

Chronic inflammation plays a significant role in the pathophysiology of CVDs, particularly in cancer patients, where it may exacerbate existing cardiovascular risks. Inflammatory cytokines such as TNF-α, IL-6, and C-reactive protein (CRP) are often elevated in cancer patients, contributing to a prothrombotic state and endothelial damage, which may accelerate the development of atherosclerosis^[5,6]. These cytokines are thought to modulate myocardial remodeling, myocyte hypertrophy and apoptosis, decreased contractility, increased fibrosis, and other adverse structural changes leading to the development of heart failure^[14]. Therefore, cancer patients who have underlying cardiovascular risk factors are at an increased risk due to the amplified effects of chronic inflammation, which elevates the likelihood of mortality from both CVDs and cancer. The impact of chronic inflammation on cardiovascular health in cancer patients raises important questions about the potential origins and maintenance of this inflammation, leading us to explore the significant role of chronic stress and its connection to both CVD and psychological disorders through shared inflammatory pathways.

Inflammation as a link between chronic stress, CVD, and psychological disorders

Various conditions, including cancer, may act as a source of significant physiological and psychological stress. Chronic stress disrupts the body’s homeostasis by activating the hypothalamic-pituitary-adrenal axis and sympathetic nervous system (SNS), resulting in the release of glucocorticoids and catecholamines. The catecholamines, particularly norepinephrine, upregulate the production of pro-inflammatory cytokines such as IL-1 beta, IL-6, TNF-α, and CRP. The glucocorticoids, on the other hand, exert an anti-inflammatory effect^[15].

However, over time, glucocorticoid resistance develops, thereby promoting a state of unregulated low-grade chronic inflammation. This is associated with endothelial dysfunction, altered vascular reactivity, and enhanced coagulation, contributing to the development of CVDs such as hypertension and atherosclerosis^[6,15]. Additionally, it aids the development of other conditions, including depression and obesity. Depression further promotes unhealthy behaviors like alcohol consumption, smoking, and physical inactivity, worsening cardiovascular health^[15–17]. The sustained inflammatory response is believed to have a role in the development of symptoms of depression. This is supported by the fact that patients with severe depression have been found to have high circulating levels of pro-inflammatory cytokines, especially TNF-α and IL-6^[16]. Given the widespread impact of stress, addressing both its physiological and psychological effects is crucial for improving public health and reducing the burden of stress-related diseases (Fig. 1).

Figure 1.

Inflammatory pathways involved in anthracycline-mediated cardiotoxicity.

To conclude, inflammation has been implicated in the pathophysiology of cardiotoxicity, CVDs, and psychological disorders in cancer patients. Addressing inflammation through targeted interventions could be key to reducing the long-term health burden and improving outcomes for cancer survivors.

The drug enters cells, interacting with the nucleus and mitochondria. In the nucleus, it inhibits topoisomerase 2 beta, preventing DNA ligation, and intercalates with DNA, causing breaks that activate the p53 gene, leading to pyroptosis. This process releases DAMPs, activating the immune system. Anthracycline also disrupts mitochondrial function by binding to Complex I, inhibiting the electron transport chain, causing uncoupling, and reducing ATP synthesis. Additionally, it intercalates with mitochondrial DNA and binds free iron, promoting extensive redox cycling and ROS production. ROS initiates an inflammatory response, causing a release of proteolytic enzymes that damage the myocardium. DAMPs bind to Toll-like receptors, causing NF-kB translocation to the nucleus, initiating transcription of pro-inflammatory cytokines. Furthermore, anthracycline activates the NLRP3 inflammasome, initiating downstream signaling pathways involving caspase 1 that promote pro-inflammatory cytokine production, inflammation, and cell death. Anthracycline also inhibits COX-2 and LOX enzymes, which have an anti-inflammatory role.

Biomarkers of inflammation in cardio-oncology and psychological disorders

Key inflammatory biomarkers: CRP, IL-6, TNF-α, and their role in predicting cardiotoxicity and psychological distress.

The inflammatory triad (CRP, IL-6, TNF-α) shares key roles in cardio-oncology and psychological disorders:

CRP

Sensitive predictor of trastuzumab-induced cardiotoxicity in women with early-stage breast cancer^[17]. Associated with CVD risk in rectal cancer^[18] and secondary cancers (e.g. non-germ cell tumor)/CVD in testicular cancer survivors(≥1.5 mg/L)^[19].

IL-6 is a key biomarker in the inflammatory response linked to cardiotoxicity. It drives cardiotoxicity in immune checkpoint inhibitors (ICIs) therapy (e.g. PD-L1/CTLA-4 and PD-1/LAG-3 associated myocarditis)^[20]. Validated in multicenter studies (e.g. JACC: CardioOncology 2023) for early cardiotoxicity detection when combined with troponin and natriuretic peptides^[21]. Targeted by IL-6 inhibitors and corticosteroids to reduce ICI-related myocarditis and arrhythmias^[10].

• TNF-α mediates cachexia, sarcopenia, and cardiac wasting during cancer treatment^[22]. In gastric cancer, it facilitates a pro-cancer microenvironment by activating the NF-κB pathway^[23].

Potential use of biomarkers for early detection and risk stratification

Clinical example

In the HERA trial, baseline hs-CRP >3 mg/L identified breast cancer patients with a 2.3-fold higher risk of trastuzumab-induced cardiotoxicity (P = 0.004)^[17].

Biomarkers are crucial for the early detection and risk stratification of inflammation-related complications in cardio-oncology. IL-6, a cytokine involved in both pro- and anti-inflammatory responses, is linked to conditions like depression and schizophrenia^[24]. Elevated IL-6 levels, alongside TNF-α, are associated with inflammation and increased CVD risk, aiding early identification of at-risk patients^[25].

Additionally, CRP and other inflammatory markers are key in assessing long-term health risks, particularly in populations exposed to environmental stressors like firefighters, indicating systemic inflammation linked to cardiovascular and respiratory diseases^[26].

Serum cytokines, like IL-1α and IL-6, in cancer patients highlight the need for a broader range of biomarkers to assess cancer-related cognitive changes and cardiovascular risks, emphasizing the complexity of inflammation in cancer therapy^[27].

One example of the role of cytokines in cardiotoxicity is that IL-2 therapy can cause temporary heart dysfunction and increase the risk of arrhythmias and heart attacks in patients treated^[28,29].

Psychological stress can significantly worsen cardiovascular risks when combined with inflammatory processes. Chronic stress elevates inflammatory biomarkers like IL-6 and TNF-α, amplifying risks of chemotherapy-induced cardiotoxicity. Cardiovascular biomarkers like NT-proBNP and high-sensitivity troponins are critical for assessing cardiac risk, reflecting hemodynamic overload and cardiomyocyte damage^[30]. A holistic approach integrating biomarkers, psychological support, and personalized care is essential to improve outcomes, especially considering the shared pathophysiological factors between cancer, heart failure (HF), and mental health challenges like depression and anxiety, which are often exacerbated in cancer patients^[31,32]. In summary, CRP, IL-6, and TNF-α serve as shared biomarkers for predicting cardiotoxicity and psychological distress in cancer patients, supporting integrated care.

Role of pain management in modulating inflammation and cardiovascular risk

Impact of perioperative pain management strategies on inflammation

Opioids play a central role in managing cancer-related pain, providing powerful analgesia that helps preserve patients’ QOL. While they are primarily used for acute and severe pain, long-term administration is common in those with persistent symptoms^[33]. In acute settings, such as perioperative pain management, strategies involving opioids may influence the inflammatory response, as these agents can induce acute cardiovascular effects such as hypotension, orthostatic instability, syncope, and bradycardia, potentially impacting systemic inflammation^[34,35]. Given these potential risks, their use requires a careful balance between effective pain control and minimizing adverse cardiovascular outcomes.

Non-steroidal anti-inflammatory drugs (NSAIDs) exert their therapeutic effects through the modulation of inflammation, but this modulation comes at a cost, particularly regarding cardiovascular safety^[36]. As shown previously in interventional and observational studies, NSAIDs are associated with an increase in cardiovascular risk, thrombotic events, elevated blood pressure, congestive HF, and palpitations^[36]. However, considerable variability exists among individual NSAIDs, with the patient’s baseline cardiovascular risk significantly influencing their safety^[36,37]; high-quality evidence on their analgesic efficacy in cancer pain is limited due to short study durations and heterogeneity in outcome measures^[38].

Regional anesthesia (RA) plays a crucial role in enhancing cardiovascular stability during the perioperative period by mitigating the systemic stress response associated with surgery. These effects are particularly beneficial for high-risk populations, such as elderly patients or those with preexisting cardiovascular conditions, as they help minimize the risk of perioperative complications^[39]. Furthermore, RA is hypothesized to improve long-term cancer outcomes by reducing surgical stress and immunosuppression, decreasing the need for volatile anesthetics and opioids, and ultimately mitigating pro-tumor pathways activated during the perioperative period^[40].

Influence of pain control on psychological well-being and cardiovascular health in cancer patients

Pain management and psychological stress in cancer patients are closely interconnected, as emotional distress can amplify pain perception, while effective pain control helps alleviate psychological stress. Therefore, incorporating psychological assessments and interventions into cancer pain management protocols is essential. In this context, multidisciplinary teams play a crucial role by integrating analgesic treatment with psychological and behavioral approaches, ensuring a comprehensive strategy for symptom management and improving patient well-being^[41,42].

Uncontrolled pain in cancer patients can contribute to increased cardiovascular risk, particularly when considering that chronic pain is associated with heightened SNS activity, which can lead to increased heart rate, blood pressure, and vascular resistance, thereby elevating cardiovascular risk^[43]. In addition, chronic pain patients face associated lifestyle changes. As shown previously in a cohort study, older adults with chronic pain often experience significant reductions in physical activity, declines in mental health, sleep quality, and diet, all of which can further intensify their pain experience^[44].

In the context of cancer care, a multidisciplinary approach integrating pharmacological and psycho-behavioral pain treatments, including strategies like reframing negative thoughts and leveraging social support, is crucial for managing chronic cancer-related pain, as highlighted by patient experiences and preferences^[45]. Furthermore, the American Society of Clinical Oncology guidelines recommend mindfulness-based interventions, yoga, relaxation, music therapy, reflexology, and aromatherapy in patients with active cancer treatment and the post-treatment period to reduce anxiety and depression symptoms^[46].

Therapeutic strategies targeting inflammation

Pharmacological Approaches

NSAIDS – with nitric oxide (NO) donating aspirin formulations for the prevention of CVD supported the pro-apoptotic^[47–50] anti-proliferative^[47] pro-oxidant^[51], and inhibition of mitogen-activated protein kinase pathways^[52,53] effects, and possible NO donating NSAIDs application in the prevention and treatment of a variety of different cancers^[54]. The over-expression of NSAID-activated gene (NAG-1) in cancer cells results in growth arrest and an increase in apoptosis, suggesting that it can act as a tumor suppressor in the early stages of tumor progression, and the expression of NAG-1 can be increased by the COX-II inhibitors^[55]. In recent years, an increasing number of studies have indicated that NSAIDs, such as Celecoxib, Meloxicam, Sulindac, Aspirin, Sildenafil, Rofecoxib, and Sodium Salicylate, have diverse effects in cancer that are mediated by the autophagy pathway. Molecular and cellular potential targets were selected for pre-clinical and clinical studies to prove the therapeutic function of NSAIDs in the management of neurodegenerative diseases^[56–59]. Immunomodulators – there have been reports on immunomodulating properties of several commonly used drugs, statins, metformin, and Angiotensin II Receptor Blockers (ARB), which can be used to treat or prevent cancer. Among anticancer drugs, anthracyclines, immunomodulatory drugs (IMiDs), and epigenetic drugs not only kill the cancer cells directly, but also enhance the immune system to attack the cancer cells. It will be beneficial to combine these drugs with conventional cancer therapies to achieve better outcomes^[60,61].

Pharmacological approaches include NSAIDs, especially NO donating formulations. These drugs also influence NAG-1 expression, contributing to tumor suppression and may engage the autophagy pathway. Immunomodulators, statins, metformin, and ARBs, as well as anticancer drugs, notably anthracyclines and epigenetic agents.

Non-pharmacological approaches

Lifestyle interventions – low-grade chronic inflammation has been associated with the risk of several chronic diseases, including CVD and several cancers^[62]. It is therefore important to understand how one may reduce inflammation, as it is possible that reducing inflammation may represent a feasible disease-prevention strategy. Several modifiable factors have been associated with reduced inflammation, including: • increased dietary fiber intake^[63] • decreased saturated fat intake^[64] • increased physical activity^[65] • not smoking^[66] • moderate alcohol consumption^[67] • and use of certain supplements and drugs: glucosamine^[68,69], chondroitin^[68,69], fish oil^[68,70], vitamin E^[71], statins^[72], and aspirin^[73].

In addition to lifestyle changes, herbal medications like Traditional Chinese medicine (TCM), especially Chinese herbal medicines and acupuncture, have been traditionally used to treat patients in China and other East Asian countries. Numerous studies have indicated that TCM alleviates the symptoms (e.g. fatigue, chronic pain, anorexia/cachexia, and insomnia) of patients with cancer and improves their QOL^[74]. Some Chinese herbal medicines (e.g. Panax ginseng, Panax quinquefolius, Astragali radix, Bu-zhong-yi-qi-tang [TJ-41], Liu-jun-zi-tang [TJ-43], Shi-quan-da-bu-tang [TJ-48], and Ban-xia-xiexin-tang [TJ-14]) and acupuncture points (e.g. Zusanli [ST36], Zhongwan [CV12], Neiguan [PC6], and Baihui [GV20]^[75–77]).

Non-pharmacological strategies focus on lifestyle changes (e.g. diet, exercise, smoking cessation), which reduce chronic inflammation linked to chronic diseases. Supplements, as known, fish oil, vitamin E, and glucosamine will help. TCM, including herbal remedies and acupuncture, is highlighted for improving the QOL and reducing treatment side effects in cancer patients.

Emerging therapies

New cancer treatments are being developed that target inflammatory cytokines, transcription factors, and immune cells^[78]. Therapies that focus on the adaptive immune system, such as ICIs like pembrolizumab and nivolumab, have already shown success. This highlights the need to better understand the role of inflammation and the innate immune system in cancer. Targeting components like macrophages, dendritic cells, or cytokines, IL-1, and TNF-α could offer new opportunities^[79,80]. Combining therapies that engage both the adaptive and innate immune systems within the tumor microenvironment may lead to more effective treatments.

Clinical implications and future directions

As in many areas of medicine, bridging the gap between evidence-based medicine and clinical application remains a significant challenge in cardio-oncology. The complexity of integrating cardioprotective strategies into oncology care is compounded by limited funding, regulatory hurdles, and the need for large-scale clinical trials. Additionally, disparities in healthcare infrastructure, variability in provider expertise, and patient adherence to long-term cardiovascular monitoring further hinder implementation^[81]. Addressing these challenges demands interdisciplinary collaboration, standardized guidelines, and continued investment in translational research to improve patient outcomes^[82].

A comprehensive, patient-centered approach is essential for effectively managing inflammation, cardiovascular health, and psychological well-being in cancer patients. Integrating conventional medical treatments with evidence-based complementary therapies and lifestyle modifications (such as stress management, improved sleep hygiene, balanced nutrition, and regular physical activity) can enhance treatment outcomes and overall QOL^[81]. A holistic model calls for a comprehensive post-diagnosis assessment for each patient, including an initial psycho-oncological evaluation to gauge distress levels and a structured lifestyle review to identify psychological or physical factors that could impact treatment adherence and long-term prognosis^[83,84]. By addressing these interconnected health domains early, an integrative approach can help mitigate the adverse effects of inflammation while supporting both cardiovascular and mental health in oncological care.

Advancing our understanding of inflammation in cardio-oncology and psychological disorders is essential for developing more effective and personalized treatment strategies. Future research should focus on key areas:

Inflammatory biomarkers

Future research in cardio-oncology and psychological disorders should explore how inflammation drives disease progression and treatment response, aiming to identify novel biomarkers for early risk stratification and personalized interventions. Cohort studies have linked several inflammatory biomarkers, such as leukocytes, haptoglobin, CRP, and immunoglobulin G, to psychiatric disorders^[85,86]. Similarly, further investigation is needed into cardiotoxicity biomarkers to enable early detection before irreversible damage occurs; among the most critical biomarkers are cardiac troponin and natriuretic peptides^[22,87].

Artificial intelligence based approaches

Advancements in artificial intelligence (AI) and machine learning may optimize patient-specific treatment algorithms, improving outcomes in high-risk populations^[88]. Moreover, interdisciplinary collaborations between cardiologists, oncologists, and mental health specialists will be essential to developing comprehensive, patient-centered care models.

Anti-inflammatory therapies

Future studies should also explore the impact of anti-inflammatory therapies, including biologic and lifestyle interventions, in mitigating both cardiovascular and psychological comorbidities^[89-91].

A precision medicine framework will ultimately enhance patient outcomes by addressing inflammation-driven pathophysiology with targeted, individualized treatments.

Conclusion

Inflammation plays a major role in the development of cancer, heart disease, and psychological disorders. Research shows that it worsens the side effects of cancer treatments on the heart, promotes tumor growth, and also impacts mental health.

Despite this knowledge, many current treatments do not fully address the widespread effects of chronic inflammation, leading to less-than-ideal outcomes. It is important to deepen our understanding of how inflammation affects the mind, heart, and body to develop more precise and effective therapies.

There is a growing need for new approaches that target the complex ways chronic inflammation works in the body. Strategies such as improving lifestyle habits, using traditional medicine (like Chinese herbal therapies), and carefully applying drugs like NSAIDs and immunomodulators can provide valuable support alongside standard treatments.

Looking ahead, tools like AI, advanced biomarker testing, and collaboration between different specialties will be key to creating personalized care plans. By adopting a more holistic, inflammation-focused model, we can improve the QOL for cancer survivors, protect heart health, and promote mental well-being, shaping a better future for cancer and heart care.

Ethical approval

Ethics approval was not required for this review.

Consent

Consent was not required for this review.

Sources of funding

Funding was not required for this review.

Author contributions

S.S.B. conceptualized the study, coordinated the writing process, and finalized the manuscript. All authors (S.S.B., D.C.C., T.B., S.Y., K.V., A.P., S.I., and J.K.) contributed to writing and revising the manuscript. J.K. served as the corresponding author. All authors reviewed and approved the final manuscript.

Conflicts of interest disclosure

No conflict of interest.

Research registration unique identifying number (UIN)

Not applicable.

Guarantor

Shreya Singh Beniwal.

Provenance and peer review

Not applicable.

Data availability statement

All data are online.