Epicardial adipose tissue secretes adipocytokines via paracrine mechanisms to impact cardiac function, serving as a potential therapeutic target for heart failure with preserved ejection fraction.
Epicardial adipose tissue plays a significant role in the pathogenesis of HFpEF through paracrine mechanisms and represents a potential therapeutic target.
With the evolving landscape of diseases, heart failure with preserved ejection fraction (HFpEF) now encompasses more than half of all heart failure patients. This condition is clinically diverse, involving multiple organ systems and often occurring alongside the aging process. To deeply investigate the common pathogenesis of HFpEF and to explore new therapeutic approaches is of great significance for the treatment of HFpEF. Epicardial adipose tissue (EAT) is not only a dynamic organ with biological functions but also physically adjacent to the myocardium and coronary arteries, endowing it with unique properties as a visceral fat depot. During pathology, EAT can secrete adipocytokines via paracrine mechanisms, establishing direct communication with the heart and vascular, thereby impacting cardiac function. This review aims to elucidate the intricate relationship between EAT and cardiac function in HFpEF, delineate the roles of adipocytes, macrophages, lymphocytes, and stem cells within EAT in HFpEF, and summarize the progress in research regarding drug therapies targeting EAT for HFpEF treatment.
Qi et al. (Sat,) conducted a review in Heart failure with preserved ejection fraction (HFpEF). Drug therapies targeting epicardial adipose tissue (EAT) was evaluated. Epicardial adipose tissue secretes adipocytokines via paracrine mechanisms to impact cardiac function, serving as a potential therapeutic target for heart failure with preserved ejection fraction.
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