Fibroblast growth factor receptor: Bidirectional regulatory role and therapeutic potential in cardiovascular disease

Cardiovascular disease (CVD) is the main cause of global incidence rate and mortality. Its pathogenesis and progression are closely related to various molecular mechanisms. The fibroblast growth factor receptor (FGFR) family is an important member of receptor tyrosine kinases, playing a crucial role in the physiological and pathological processes of the cardiovascular system. Through interaction with ligands, FGFR regulates vascular remodeling, inflammatory response, cell metabolism and tissue repair, thus affecting the progress of atherosclerosis, hypertension, atrial fibrillation (AF), left ventricular hypertrophy (LVH) and related CVDs. While FGFR demonstrates therapeutic promise in attenuating disease progression, its pathophysiological mechanisms across diverse cardiovascular pathologies remain incompletely understood. Notably, emerging evidence indicates a paradoxical dual regulatory role: FGFR may exert inhibitory effects on disease pathogenesis in specific contexts, whereas it also can facilitate pathological progression through specific signaling cascades under alternative pathophysiological conditions. This highlights the need to delineate the specificity of the FGFR signaling pathway and its interactions with other molecular networks in future research to optimize targeted intervention strategies and evaluate their safety and effectiveness in clinical applications. This review delineates the regulatory roles of FGFRs in CVDs, focusing on their involvement in pathological mechanisms spanning vascular remodeling and myocardial dysfunction. By analyzing contradictory therapeutic effects and subtype-dependent interactions, it identifies key challenges in reconciling FGFRs' protective and disease-promoting effects. These findings underscore the imperative to refine therapeutic approaches targeting FGFR-mediated signaling networks to advance CVD management strategies.