VEGF-B Promotes Endocardium-Derived Coronary Vessel Development and Cardiac Regeneration

Background: Recent discoveries have indicated that, in the developing heart, sinus venosus and endocardium provide major sources of endothelium for coronary vessel growth that supports expanding myocardium. Here we set out to study origin vessels develop response vascular endothelial factor B (VEGF-B) heart effect VEGF-B on recovery from myocardial infarction. Methods: We used mice rats expressing a transgene, VEGF-B-gene–deleted rats, apelin-CreERT, natriuretic peptide receptor 3–CreERT recombinase-mediated genetic cell lineage tracing viral vector–mediated gene transfer adult mice. Left anterior descending ligation was performed, 5-ethynyl-2’-deoxyuridine–mediated proliferating cycle labeling; flow cytometry; histological, immunohistochemical, biochemical methods; single-cell RNA sequencing subsequent bioinformatic analysis; microcomputed tomography; fluorescent- tracer-mediated perfusion imaging analyses were development function VEGF-B–induced heart. Results: show cardiomyocyte overexpression during promotes novel originate directly cardiac ventricles maintain connection with subendocardial In mice, proliferation induced by located predominantly vessels. Furthermore, transduction before or concomitantly left artery promoted endocardium-derived into myocardium improved tissue remodeling function. Conclusions: The transgene formation development, structural functional rescue after could new therapeutic strategy neovascularization occlusion most vulnerable tissue.