Table 3.

Future perspectives on drugs targeting EAT.

Treatment with Potential Effect on EAT	Rationale	Evidence
Statins	Pleiotropic effect (especially on myocardial inflammation)	Reduction in EAT-secreted inflammatory mediators [72] Improvement in cardiac remodeling in rats [71]
Anticytokines (e.g., anti-TNF alpha, anti-IL1)	Reduction in systemic inflammation	Indirect (and controversial) evidence on reduction in systemic inflammatory biomarkers with hypothesis-generating data [74,75,76,77,78,79]
SGLT2 inhibitors	Reduction in cardiac inflammation and fibrosis	Reduction in EAT mass and fibrosis and inflammatory biomarkers [85,86]
Other oral antidiabetic agents (e.g., metformin, GLP1-RA)	Anti-inflammatory and anti-oxidative stress effects, role on adipogenesis and adipocyte function	Reduction in EAT mass and EAT-related inflammation with hypothesis generated through controversial data
Fibroblast growth factor 21 gene therapy	Improvement in energy homeostasis in visceral adipose tissue	Intraperitoneal injection associated with lower adiposity, inflammatory cytokines, insulin resistance, and glycemic processing in mice [89]

EAT: epicardial adipose tissue; SGLT2: sodium glucose transporter 2; GLP1-RA: glucose lowering protein 1 receptor agonist.