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Article Abstract
Following myocardial infarction (MI), endothelial cell proliferation drives neovascularization to support cardiac regeneration. While myeloid-derived growth factor (Mydgf) is known to promote cardiac repair post-injury, yet its mechanism in angiogenesis remained unclear. In this study, we found that myeloid-derived growth factor knockout (Mydgf-KO) reduced endothelial cell proliferation during early postnatal cardiac angiogenesis and impaired neovascularization post-MI, leading to exacerbated cardiac dysfunction. Recombinant MYDGF therapy reversed these deficits. Liquid chromatography mass spectrometry analysis (LC-MS) analysis of cardiac ECM in Mydgf-KO mice revealed FGF1 as a critical downstream effector of Mydgf in angiogenesis. Administration of recombinant FGF1 protein significantly promoted endothelial cell proliferation and tube formation in human coronary artery endothelial cells. These findings establish the Mydgf-FGF1 axis as a critical regulator of cardiac angiogenesis and unveil its promise as a therapeutic target to promote vascular repair in ischemic heart disease.
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