Role of epicardial adipose tissue in heart failure with preserved ejection fraction: An emerging molecular mechanism and therapeutic potential.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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