Abstract
Epicardial fat (EAT) is the visceral fat depot of the heart. Given its rapid metabolism, organ fat specificity, and simple objective measurability, epicardial fat can serve as a target for pharmaceutical agents targeting the adipose tissue. EAT has shown to significantly respond to thiazolidinediones (TZD), glucagon-like peptide-1 receptor (GLP-1R) agonists, sodium-glucose cotransporter 2 inhibitors (SGLT2i), dipeptidyl peptidase-4 inhibitors (DPP4i), and statins. EAT may represent a measurable risk factor and modifiable therapeutic target. Targeted pharmaceutical interventions may allow EAT to resume its physiological role. A drug-induced browning effect on EAT suggests the development of pharmacological strategies to increase energy consumption. The potential of modulating the EAT transcriptome with targeted pharmacological agents can open new avenues in the pharmacotherapy of cardiometabolic diseases.