Front Cardiovasc Med. 2026 Jul 27;13:1843719. doi: 10.3389/fcvm.2026.1843719. eCollection 2026.
ABSTRACT
BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) and coronary artery disease (CAD) are interconnected global health epidemics that substantially contribute to worldwide morbidity and mortality. We aimed to provide a systematic overview of the epidemiological links and shared pathophysiological mechanisms between MASLD and CAD, evaluate emerging therapeutic strategies with dual benefits, and advocate for an integrated "dual-heart-liver" management model.
METHODS: We synthesize current evidence to examine the epidemiological link between MASLD and CAD and their shared pathophysiological mechanisms, including endothelial dysfunction, chronic inflammation, metabolic imbalance, insulin resistance, and genetic associations. We also discuss the roles of genetic predisposition, lifestyle modification, and combination therapies in improving patient outcomes. Furthermore, recent advances in pharmacotherapy-such as resmetirom, GLP-1 receptor agonists, SGLT2 inhibitors, FGF21 analogues, PCSK9 inhibitors, and PPAR agonists-are evaluated for their dual benefits on hepatic and cardiovascular health.
RESULTS: Epidemiological studies confirm a bidirectional, mutually reinforcing relationship between MASLD and CAD, which are linked through multiple pathophysiological pathways. In terms of treatment, novel pharmacotherapies-such as resmetirom, GLP-1 receptor agonists, SGLT2 inhibitors, FGF21 analogues, PCSK9 inhibitors, and PPAR agonists-show considerable potential for conferring concurrent hepatic and cardiovascular benefits. Furthermore, combination therapies also play important roles in optimizing patient outcomes.
CONCLUSIONS: This review calls for a paradigm shift toward an integrated "dual-heart-liver" management model, emphasizing the need for systematic cardiovascular risk assessment in MASLD patients and the implementation of collaborative care strategies to improve long-term prognosis.
PMID:42577170 | PMC:PMC13453754 | DOI:10.3389/fcvm.2026.1843719