Asprosin as a Molecular Switch in Epicardial Adipose Tissue Remodeling and Cardiometabolic Disease: New Insights

Epicardial adipose tissue (EAT) is a specialized visceral fat depot that directly interfaces with the myocardium. Under physiological conditions, EAT exhibits a beige-like thermogenic phenotype with enhanced angiogenesis and an anti-inflammatory secretome, contributing to cardioprotection. However, metabolic stress associated with obesity and type 2 diabetes mellitus disrupts this homeostasis, promoting EAT whitening, vascular dysfunction, hypoxia, fibrosis, and chronic inflammation, ultimately leading to adverse cardiovascular outcomes. Asprosin, a recently characterized fasting-induced adipokine, is an important regulator of systemic glucose metabolism, appetite, and insulin resistance. Experimental evidence suggests that asprosin suppresses adipose browning by downregulating thermogenic pathways while promoting adipogenesis and lipid accumulation. This review proposes an integrated asprosin-EAT whitening-angiogenesis axis as a conceptual framework linking EAT dysfunction and cardiovascular disease. Asprosin may contribute to phenotypic remodeling of epicardial adipose tissue through mechanisms involving impaired adipose browning, altered angiogenesis, and vascular dysfunction. Further investigation of the local and paracrine actions of asprosin within EAT is required to determine its potential as a biomarker and therapeutic target for cardiometabolic disease.