Potentials of SGLT2 inhibitors in the treatment of diabetic rotator cuff diseases: a comprehensive review

Abstract

Degenerative rotator cuff disease (RCD) is a common musculoskeletal condition that disproportionately affects individuals with diabetes mellitus, leading to pain, functional impairment, and a reduced quality of life. Emerging evidence suggests that sodium-glucose co-transporter 2 inhibitors (SGLT2is), which are widely used for glycemic control in type 2 diabetes, offer additional musculoskeletal benefits beyond their metabolic effects. This review explores the potential protective role of SGLT2is in diabetic RCD by examining the epidemiological link between diabetes and tendon degeneration and evaluating the biological mechanisms through which SGLT2 is influence tendon health. These potential benefits include reducing inflammation, altering metabolism to a more tendon-friendly state, combating oxidative stress with ketones, encouraging a healing environment through macrophage modulation, and improving overall health via weight and blood sugar management. Preclinical and observational studies provide preliminary support for therapeutic benefits, although high-quality randomized clinical trials are lacking. Understanding the multifaceted role of SGLT2is in tendon biology will open new avenues for prevention and management of RCD, particularly in patients with metabolic disorders.

INTRODUCTION

Musculoskeletal disorders are becoming increasingly prevalent, affecting individuals' quality of life and placing a considerable burden on healthcare systems [1]. Rotator cuff disease (RCD) is the most common musculoskeletal disease occurring around the shoulder. This condition has attracted significant attention due to its considerable impact on patients' daily lives and functional abilities. [2]. As the incidence of this condition continues to increase, there is an urgent need to investigate novel approaches to prevent and manage rotator cuff tears and facilitate subsequent repair surgeries [3].

RCD is characterized by a group of conditions that affect the rotator cuff, a complex structure composed of muscles and tendons surrounding the shoulder joint [2,3]. Patients with RCD often face physical limitations and emotional distress, underscoring the importance of innovative and effective treatment strategies [1,3,4]. Recent research has demonstrated a significant association between diabetes mellitus and increased risk of RCD (Fig. 1). Patients with diabetes are more susceptible to rotator cuff tears, which often require surgical repair [4,5]. Furthermore, individuals with poorly controlled diabetes exhibit a greater rate of rotator cuff re-tears after repair surgery [6].

Fig. 1.

Schematic diagram of mechanisms of diabetic rotator cuff disease and the potential role of sodium-glucose co-transporter 2 inhibitors (SGLT2is). This illustrates how chronic hyperglycemia promotes tendon degeneration through advanced glycation end-products, collagen cross-linking, and matrix breakdown, leading to tendinopathy and rotator cuff tears. It also highlights the potential benefits of SGLT2is in mitigating these effects via glycemic control, anti-inflammatory actions, ketone metabolism, and tendon regeneration. Adapted from PubChem (https://pubchem.ncbi.nlm.nih.gov).

Therefore, it is critical to investigate the role of diabetic medications in potential protective interventions against RCD [5,6]. Among these interventions, sodium-glucose co-transporter 2 inhibitors (SGLT2is) have garnered attention because of their anti-inflammatory properties, potential to facilitate weight loss, and ability to reduce glucose levels [7,8]. Commonly known as gliflozins (e.g., canagliflozin, dapagliflozin, and empagliflozin), SGLT2is are primarily used to manage type 2 diabetes mellitus [8,9]. These drugs inhibit SGLT2 proteins in the renal proximal tubules, reducing glucose reabsorption and promoting urinary excretion of glucose, which subsequently lower blood glucose levels and improve glycemic control [7,9-11].

Some studies have suggested that SGLT2is help prevent RCD, possibly owing to their anti-inflammatory effects [12], support in weight reduction, and improved glycemic management [11,12]. Although the exact mechanisms remain under investigation, early evidence indicates a reduced risk of tendon rupture and tendinitis in individuals using SGLT2is compared to those on other diabetes medications [12]. This points to a complex relationship between diabetes and musculoskeletal health and highlights the need for further investigation to uncover the mechanisms connecting these conditions [3,5,6]. Additional research is essential to better understand the role of SGLT2is in preventing RCD, compare their effects with those of other antidiabetic agents, and explore the benefits of specific subtypes.

EPIDEMIOLOGY AND PREVALENCE OF DEGENERATIVE RCD

Given the global burden of RCD as outlined, understanding its link with diabetes provides a critical foundation for exploring the therapeutic pathways of diabetic medications, particularly SGLT2is [1-4]. Understanding the global impact of RCD is crucial when exploring potential preventive strategies, such as the connection between diabetes and SGLT2is [7,8]. Statistics illuminate the staggering global reach of RCD. A cross-sectional study conducted in the United Kingdom, revealed that 28.8% of the general population seeking for a medical attention for shoulder pain [13]. This statistic highlights the global burden of shoulder pathology, suggesting that many individuals across regions experience pain, functional impairment, and diminished quality of life due to RCD [2,3,13].

The diagnostic process often involves imaging studies and specialist evaluations, followed by treatment with physical therapy, corticosteroid injections, or surgical repair [3,4,13]. The high prevalence of RCD adversely impacts productivity and leads to long-term complications, with substantial economic and social consequences [5,13].

Patients often report limitations in routine activities and reduced participation in social or occupational tasks, which can lead to psychological effects, such as isolation and depression [5,6]. Addressing RCD remains a global challenge requiring multidisciplinary strategies, and, while SGLT2is show promise, further studies are needed to validate their impact on RCD incidence [11,14,15].

PREVENTATIVE STRATEGIES

Building upon epidemiological insights, early intervention in RCD is critical, particularly given that a substantial proportion of patients with shoulder pain exhibits full-thickness tears, a severe form of tendon degeneration [13]. Preventive measures, including lifestyle modifications, weight control, metabolic monitoring, and pharmacological strategies, could help slow the progression of RCD. Implementation of such strategies could reduce the pressure on healthcare systems and enhance patient outcomes. Research on the prevalence and natural history of RCD continues to inform the development of targeted healthcare interventions, providing a roadmap for managing this increasingly common musculoskeletal condition [1,3,13].

SGLT2is

SGLT2is, a class of antidiabetic drugs with diverse chemical structures, have been extensively studied and are currently at varying stages of clinical application [8,11,14,15]. The U.S. Food and Drug Administration has approved several notable C-glycosides, such as canagliflozin, dapagliflozin, and empagliflozin, as innovative agents for type 2 diabetes management (Fig. 2). These drugs can be used as monotherapy or in combination with other antidiabetic medications, such as metformin, sulfonylureas, thiazolidinediones, and insulin [8,11,14-16]. Recent studies suggest that, beyond glycemic control, SGLT2is confer benefits in degenerative diseases, including renal, cardiovascular, neurological, and musculoskeletal conditions [5,7]. Although primarily evaluated for their glucose-lowering and cardiovascular benefits, emerging evidence supports their anti-inflammatory, antioxidative, and metabolic regulatory properties, which could extend their therapeutic potential to tendon and joint health [16-18].

Fig. 2.

Chemical structures of four U.S. Food and Drug Administration-approved C-glycosides. (A) Sotagliflozin, (B) dapagliflozin, (C) empagliflozin, and (D) canagliflozin. Adapted from PubChem (https://pubchem.ncbi.nlm.nih.gov).

The anti-inflammatory effects of SGLT2is are thought to be mediated through the suppression of pro-inflammatory cytokines, inhibition of the nuclear factor kappa B (NF-κB) pathway, and modulation of oxidative stress [17,18]. These attributes are particularly relevant in conditions characterized by chronic inflammation and tissue degeneration, such as RCD. SGLT2is may also influence key cellular pathways involved in tendon homeostasis, such as lipid metabolism, macrophage polarization, and low-grade ketone elevation. Preliminary studies suggest that these effects collectively attenuate the progression of tendon degeneration and support repair mechanisms [19,20]. Although these findings are promising, large-scale clinical trials specifically investigating their role in musculoskeletal and rotator cuff health are limited. Therefore, further investigation is warranted to validate these effects in orthopedic contexts and to distinguish their benefits from those of other antidiabetic classes.

RCD AND SGLT2is

While traditionally prescribed for glycemic control, SGLT2is have recently shown promise in managing musculoskeletal complications associated with diabetes, including RCD [21,22]. Several mechanisms have been proposed to explain these effects, including anti-inflammatory modulation through the suppression of pro-inflammatory cytokines and inhibition of the NF-κB signaling pathway, which plays a central role in mediating inflammation. Additionally, improved lipid metabolism and enhanced ketone body production contribute to metabolic homeostasis. Another important mechanism is the polarization of macrophages toward the M2 anti-inflammatory phenotype, which supports tissue repair and reduces chronic inflammation. Benefits also include weight reduction and improved glucose control, both of which are critical in mitigating metabolic and inflammatory disorders [21,23]. Chronic low-grade inflammation contributes to tendon degeneration and tear susceptibility in RCD [21,24].

SGLT2is reduce systemic inflammation through enhanced lipid handling and oxidative stress mitigation—which may have downstream effects on tendon biology [25]. Additionally, their combination with glucagon-like peptide-1 (GLP-1) receptor agonists has been shown to enhance weight loss, a relevant benefit given the strong correlation between elevated body mass index and risk of rotator cuff tears [21,24]. Although direct evidence is limited, improved glycemic control with SGLT2i use may mitigate diabetes-induced changes in tendon microcirculation, collagen cross-linking, and oxidative damage—factors implicated in poor tendon healing and re-tear risk [26]. Taken together, these findings suggest SGLT2is as a promising adjunct for management of RCD in patients with diabetes. However, well-designed randomized controlled trials (RCTs) are needed to establish causality and assess outcomes, such as tendon healing, pain reduction, and surgical success.

Consequently, it can be inferred that SGLT2is offer a comprehensive approach for managing RCD in individuals with diabetes [21]. The known benefits of these medications include reducing inflammation, promoting weight loss, and lowering glucose levels. Together, these effects may contribute to the prevention and management of rotator cuff pathologies (Table 1). Recognizing the impact of RCD on individual well-being and healthcare systems, the link between diabetes and increased risk of this condition has led to investigations of protective interventions. Additional studies are required to elucidate the mechanism by which SGLT2is promote the preservation of rotator cuff tissue [21,25]. Long-term studies and RCTs are crucial to validate the effectiveness and safety of these therapies [21].

Table 1.

Proposed mechanisms by which SGLT2is prevent or mitigate rotator cuff damage

Aspect	Description	Reference
Ketone body effects	Anti-inflammatory and antioxidant benefits for tendon health and repair	[22,61-63]
Low-grade Ketonemia	Mild ketone elevation may protect against RCD.	[21,54,64]
Anti-inflammatory	Inhibits the NF-κB pathway; modulates inflammatory cytokines	[22,62,63,65]
Antioxidant properties	Reduces oxidative stress in tendon tissues	[21,62,63,65]
Weight management	Fat loss reduces mechanical load and inflammation.	[66-70]
Glycemic control	Reduces advanced glycation end-products and tendon vulnerability	[71-73]
Chronic inflammation	Key target in tendinopathy prevention and RCD mitigation	[16,21,25]

SGLT2i: sodium-glucose co-transporter 2 inhibitor, RCD: rotator cuff disease, NF-κB: nuclear factor kappa B.

Potential Mechanisms

Emerging scientific evidence suggests that SGLT2is exert protective effects on rotator cuff tissues, particularly in individuals with diabetes mellitus, a population known to exhibit higher rates of tendon degeneration, impaired healing, and re-tears following rotator cuff repair [21]. In a real-world retrospective cohort study, Su et al. [21] reported a significantly lower incidence of rotator cuff tears and surgical repairs in patients treated with SGLT2is compared to those treated with GLP-1 receptor agonists, indicating a potential drug class–specific musculoskeletal benefit [21,27]. Although these findings are observational, they highlight a compelling need to explore the mechanistic explanations for this apparent protective association. To date, three core mechanisms have been proposed to account for the beneficial effect of SGLT2is on RCD: (1) attenuation of chronic inflammation, (2) metabolic reprogramming through enhanced fat use and ketogenesis, and (3) immunologic modulation of macrophage polarization. Collectively, these mechanisms are believed to reduce tendon degradation, foster matrix remodeling, and mitigate the deleterious systemic effects of diabetes that compromise the tendon structure and repair capacity [17,18,21,28].

Anti-inflammatory Effects of SGLT2is in RCD Prevention

One of the principal effects of SGLT2is relevant to tendon health is their potent anti-inflammatory capacity. Chronic low-grade inflammation plays a critical role in the pathogenesis of RCD, along with other degenerative tendinopathies. SGLT2is have been shown to suppress several key inflammatory pathways, particularly the NF-κB signaling cascade, which is a central regulator of pro-inflammatory gene transcription in tendinopathy [21,24,28]. In addition, SGLT2is lower circulating levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), both of which are commonly elevated in individuals with diabetes and are implicated in tendon matrix disruption and collagen breakdown [28]. By dampening these inflammatory signals, SGLT2is may prevent or delay the molecular cascade leading to rotator cuff tears and poor tendon healing.

Metabolism Reprogramming

SGLT2is, which are commonly used to manage type 2 diabetes, may also help protect tendon health by altering the body’s energy metabolism. These medications block the reabsorption of glucose in the kidneys, causing excess glucose to be excreted via urine. As a result, the body begins to use fat instead of glucose as the primary energy source [27,29-31]. This shift leads to a mild increase in ketone levels in the blood, known as low-grade ketonemia, which has been linked to reduced inflammation and oxidative stress [27,29].

Compared to glucose breakdown, fat metabolism produces fewer harmful byproducts like reactive oxygen species (ROS), which can damage tissues and promote inflammation [29,32-34]. This change creates a more favorable internal environment to maintain the tendon structure and reduce the risk of injury. In addition, fat metabolism leads to the production of specific molecules such as adiponectin and resolvins, which play important roles in controlling inflammation and promoting tissue repair [23,35,36].

Adiponectin is known to support tendon healing by stimulating collagen production and improving the strength of connective tissue through a pathway called AMPK signaling [23,37,38]. Resolvins help to actively resolve inflammation by reducing the activity of inflammatory cells and enzymes that break down tendon tissue [36,39]. Together, these molecules reduce the levels of inflammatory substances such as IL-6 and help limit tissue damage [40-42].

The observed combination of reduced inflammation and enhanced tissue repair elucidates the potential utility of SGLT2is in preventing or decelerating the progression of RCD, particularly in individuals with metabolic disorders such as diabetes [21,43]. Although preliminary studies yield promising results, larger and more targeted clinical trials are necessary to substantiate these effects in real-world patient populations [21,23,44]. Furthermore, it is imperative to investigate how variables such as individual genetic makeup, disease severity, and medication dosage affect treatment outcomes [45-47]. SGLT2is offer a novel approach for management or prevention of RCD by modifying the body’s energy metabolism and producing beneficial anti-inflammatory fat metabolites. Although further research is necessary, existing scientific evidence suggests that these medications could be beneficial not only for glycemic control but also for long-term tendon health [18,19,21,47-49].

Modulating the Macrophage Type

In addition to their metabolic and anti-inflammatory effects, SGLT2is appear to influence local immune cell behavior in a manner that supports tendon healing. Macrophages, the key immunologic regulators within tendon tissues, exhibit phenotypic plasticity and adopt either a pro-inflammatory M1 or a pro-healing M2 phenotype, depending on local signaling cues [50-52]. In diabetes and chronic tendinopathy, the balance often skews toward M1 dominance, promoting persistent inflammation and tissue degradation [53].

SGLT2is have been shown to modulate macrophage polarization, shifting the balance from an M1 toward an M2 phenotype, fostering a tissue microenvironment conducive to healing and matrix preservation [21,54-58]. This immunomodulatory action may be particularly valuable in the context of RCD, in which chronic inflammation disrupts the delicate balance between degeneration and regeneration. By promoting M2 macrophage function, SGLT2is may help restore tendon homeostasis and prevent progression toward full-thickness tears. Although these findings are promising, further research is necessary to fully understand the potential of SGLT2is for RCD prevention [21]. Initial discoveries have suggested that these medications play a key role in managing RCD by controlling diabetes and reducing tendon inflammation [21,59,60].

Ketone Metabolism

SGLT2is, although initially developed to improve glycemic control in type 2 diabetes, have demonstrated broader physiological effects, including their role in musculoskeletal health [21,54,61,64]. One notable secondary consequence of SGLT2 inhibition is the induction of low-grade ketonemia, a mild elevation in circulating ketone bodies resulting from enhanced fat oxidation and decreased insulin levels. This metabolic adaptation is increasingly recognized for its anti-inflammatory and antioxidant properties, which may contribute to the observed protective effects against RCD [21,26]. Ketone bodies, particularly beta-hydroxybutyrate, have been shown to inhibit the NF-κB pathway, a key transcriptional regulator of inflammatory cytokines involved in tendon degeneration [62,63]. Additionally, ketones serve as potent antioxidants that neutralize ROS, thereby reducing oxidative stress, which is another major contributor to tendon pathology. Collectively, these actions create a more favorable biochemical environment for tendon cell survival, matrix remodeling, and repair.

Although the precise cellular mechanisms through which ketones exert these benefits remain under investigation, their capacity to modulate redox balance and inflammatory signaling provides a plausible link between the metabolic shifts induced by SGLT2is and reduced tendon degeneration [21,64]. Apart from their biochemical signaling roles, ketones may also function as an efficient alternative energy substrate for metabolically stressed or inflamed tendon cells, promoting energy homeostasis and cellular resilience [65,66,74]. Thus, through a combination of signaling modulation and energy support, SGLT2-induced ketonemia may play a significant adjunctive role in preserving tendon health in diabetic individuals or in those with metabolic syndrome. Further research is required to validate these observations in clinical populations and to determine whether ketone-mediated effects can be leveraged therapeutically in non-diabetic individuals at risk of RCD.

Body Weight and Glycemic Control

In addition to direct anti-inflammatory and immunomodulatory effects, body weight regulation and glycemic control represent two additional pathways through which SGLT2is may contribute to the prevention of RCD [21,67]. Excess body mass index is a well-established mechanical and metabolic risk factor for RCD, increasing both the structural load on the rotator cuff and the systemic inflammatory tone [21,68,69]. SGLT2is facilitate weight reduction through several mechanisms, including urinary calorie loss via glucosuria, enhanced fat oxidation due to carbohydrate deficit, and modulation of appetite-regulating hormones [69,70]. By facilitating the excretion of glucose via the urine, these agents induce net caloric loss and promote weight reduction over time [61,75]. Moreover, studies suggest that SGLT2is alter central satiety signals through effects on hormones, such as ghrelin and GLP-1, contributing to reduced appetite and food intake [76,77]. The metabolic shift toward fat as a primary fuel source, induced by SGLT2 inhibition, further supports sustained weight loss and improved body composition [71,72].

In addition to weight loss, improved glycemic control provides further advantages to the musculoskeletal system. Persistent hyperglycemia accelerates the development of advanced glycation end-products, which disrupt collagen cross-linking and weaken tendon tensile strength to increase the risk of tendon tears [73]. By reducing blood glucose levels, SGLT2is may help limit advanced glycation end-product formation, decrease systemic oxidative stress, and reduce inflammatory signaling factors that are closely linked to the progression of RCD [21].

The combined effect of reduced mechanical stress due to weight loss and attenuated biochemical injury via improved glucose control creates a multifactorial defense mechanism against tendon degeneration. These systemic benefits complement the local actions of SGLT2is on tendon cells and immune responses and are particularly attractive for populations at a high risk of tendon injury, including those with obesity, diabetes, or prior rotator cuff pathology [15,21,26]. Although promising, these mechanisms are indirect, and RCD-specific clinical trials are lacking. Therefore, ongoing research is necessary to identify patient populations that may derive the greatest benefits from these therapies. Investigations comparing SGLT2is with other weight loss and glucose-lowering interventions are essential to determine whether their use should be tailored for musculoskeletal risk modification. Nonetheless, as our understanding of the interplay between metabolism and tendon health deepens, the role of SGLT2is in RCD prevention has become increasingly compelling. Their multi-pronged approach—targeting inflammation, oxidative stress, adiposity, and glucose toxicity—suggests a unique therapeutic potential to protect against this debilitating condition [4,13,21,69,70].

DISCUSSION

Despite encouraging preliminary findings, the precise biological mechanisms by which SGLT2is exert protective effects on rotator cuff tissues remain unclear [21]. This review sought to investigate the potential role of SGLT2is in alleviating RCD, particularly within the context of diabetes mellitus, by examining several intersecting mechanistic pathways. Specifically, this review concentrated on three principal domains: suppression of local and systemic inflammation, metabolic reprogramming that favors fat oxidation over glycolysis, and enhancement of glycemic control and weight regulation, each of which contributes directly or indirectly to tendon health.

The anti-inflammatory effects of SGLT2is are thought to involve the downregulation of key pro-inflammatory mediators such as IL-6 and TNF-α [21,24,28], as well as inhibition of the NF-κB signaling cascade [28]. These actions may reduce the chronic low-grade inflammation that is implicated in tendon degeneration and impaired healing. Concurrently, by promoting lipolysis and mild ketone production [27,29], SGLT2is shift energy metabolism from glucose to fat substrates, generating fewer ROS [29,33,34] and other pro-inflammatory metabolites. This metabolic shift ultimately creates a more favorable biochemical environment for tendon repair and may counteract diabetes-induced oxidative damage. Additionally, SGLT2is facilitate weight loss and enhance glucose homeostasis [15,21,26], which are independently associated with a lower risk of tendon injury and better post-repair outcomes in patients with diabetes.

Although other classes of antidiabetic medications, such as GLP-1 receptor agonists [21] and dipeptidyl peptidase-4 inhibitors, also possess anti-inflammatory potential, SGLT2is appear to offer a broader and more integrated therapeutic profile. Their multifaceted benefits, ranging from metabolic modulation to systemic inflammation reduction and possible tendon-specific effects, suggest their unique utility in musculoskeletal disease contexts. A real-world observational study conducted by Su et al. [21] supports this notion, showing that individuals treated with SGLT2is have a significantly lower incidence of rotator cuff tears and require fewer surgical interventions than those receiving GLP-1 receptor agonists. These findings indicate that the protective effect may be, at least in part, drug class–specific and not solely attributable to improved glycemic control.

This emerging evidence invites reconsideration of clinical decision-making in diabetes care. Currently, prescribing guidelines for antidiabetic medications emphasize cardiovascular, renal, and glycemic outcomes; however, musculoskeletal complications, such as RCD, may also merit consideration, particularly for patients with a history of shoulder pathology, tendinopathy, or occupations that place repetitive strain on the upper extremities. Integrating musculoskeletal risk into antidiabetic treatment algorithms may enhance functional outcomes and reduce disability in affected individuals.

Further mechanistic insights are provided by evidence that SGLT2is influence immune cell behavior, particularly macrophage polarization. These agents promote a shift from the pro-inflammatory M1 macrophage phenotype to the anti-inflammatory M2 phenotype [50,52,54-58], supporting resolution of inflammation and tendon tissue remodeling. In parallel, the mild ketonemia induced by SGLT2 inhibition not only contributes to energy balance but may also provide antioxidant and anti-inflammatory effects conducive to tendon preservation [21,61-65,74]. Together, these findings underscore the potential of SGLT2is to modulate the tendon microenvironment toward healing rather than degeneration. Nonetheless, high-quality clinical evidence specific to rotator cuff pathology remains scarce. Most current literature is derived from preclinical models, retrospective analyses, and indirect observations from broader metabolic studies. To date, no RCTs have prospectively evaluated tendon healing or rotator cuff function as primary endpoints in patients treated with SGLT2is.

To address this issue, future research should focus on generating robust clinical data to clarify these associations. Priorities should include longitudinal RCTs assessing tendon repair outcomes in SGLT2-treated patients [21,63,65], imaging-based studies quantifying tendon integrity and tear progression, and molecular investigations of tendon tissues exposed to SGLT2-induced metabolic and immunological shifts. Furthermore, examining the role of SGLT2is in non-diabetic individuals with metabolic syndrome and rotator cuff tendinopathy [15,21,26] may broaden the scope of their therapeutic applications.

This review did not involve studies with human participants or animals; therefore, Institutional Review Board approval and informed consent were not required.

CONCLUSIONS

SGLT2is, originally designed for glycemic control in type 2 diabetes, have demonstrated emerging potential in the prevention and management of diabetic RCD. Their anti-inflammatory effects, metabolic benefits, and support for weight reduction align with several known contributors to tendon degeneration, particularly in patients with diabetes. However, the current evidence remains preliminary. Robust clinical trials, ideally randomized and prospective, are imperative to confirm these associations, understand the underlying mechanisms, and delineate their roles relative to other diabetes medications. Furthermore, assessing the efficacy of SGLT2is in non-diabetic individuals with rotator cuff pathology or in postoperative healing contexts represents a promising direction for future research. As the intersection between metabolic health and musculoskeletal disorders continues to be explored, SGLT2is may emerge as an important component of interdisciplinary approaches to tendon care and injury prevention.