Vascular Endothelial Growth Factor B Modulates Cardiac Functions via Ferroptosis Pathways in Post-Myocardial Infarction.

ABSTRACT: Myocardial infarction (MI) remains a leading cause of mortality worldwide, yet effective cardioprotective strategies remain limited in clinical settings. Vascular endothelial growth factor B (VEGFB) has emerged as a promising therapeutic candidate in MI, but the role of its co-receptor, Neuropilin-1 (NRP1), in cardiomyocyte (CM) survival under ischemic stress remains poorly understood. Here, we investigated VEGFB-NRP1 signaling using an in vivo zebrafish model of cardiac injury as well as in vitro hypoxia models in CMs. We demonstrated that VEGFB overexpression conferred protection against ischemic injury and enhanced cardiac regeneration in the zebrafish heart. Mechanistically, we showed that VEGFB treatment enhances CM viability through reducing reactive oxygen speci

SUBMITTER: Varanasi SM 

PROVIDER: S-EPMC12562414 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature