Key result
Obese epicardial fat promotes cardiac remodeling and inflammation via female-specific hormonal and metabolic pathways.
Why the study?
Understanding sex-specific epicardial fat tissue biology is essential for personalized cardiovascular disease prevention and treatment in obesity-related disorders.
Understanding sex-specific epicardial fat tissue biology is essential for personalized cardiovascular disease prevention and treatment in women with obesity-related disorders.
May inform sex-specific risk assessment in obese women; hypothesis-generating for targeted epicardial fat therapies.
Obesity is a global health burden with significant sex-specific implications, especially in cardiovascular disease (CVD). Epicardial fat tissue (EFT), a metabolically active visceral fat depot between the myocardium and visceral pericardium, plays a critical role in cardiac health. Under normal conditions, EFT supports the heart via anti-inflammatory signaling, fatty acid metabolism, and nitric oxide–mediated vasodilation. However, in obesity and cardiometabolic syndrome, EFT becomes proinflammatory, contributing to cardiac remodeling and endothelial dysfunction. Since women experience unique hormonal and metabolic influences, risk factors such as menopause, polycystic ovarian syndrome, vitamin D deficiency, and sleep apnea are linked to increased EFT in women, independent of body mass index, and correlate with adverse cardiac remodeling and inflammation. Therapeutic strategies such as exercise, GLP-1 receptor agonists, and hormone replacement therapy show promise in reducing EFT. Understanding sex-specific EFT biology is essential for personalized CVD prevention and treatment in obesity-related disorders.
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Tzidon et al. (2025) conducted a review in Cardiovascular disease in women. Epicardial fat tissue (EFT) was evaluated. Epicardial fat tissue becomes proinflammatory in obesity, contributing to adverse cardiac remodeling and inflammation in women due to unique hormonal and metabolic influences.
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