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Angiopoietin Like protein 3 (ANGPTL3) is at present considered as a central molecular target for therapy designed to reduce atherogenic lipids and atherosclerosis. However, concerns about the safety of inactivation of ANGPTL3 in patients with coronary artery disease (CAD) especially myocardial infarction (MI) have been raised. ANGPTL3 is reported to possess proangiogenic property. Angiogenesis is critical to the recovery of MI. Endothelial progenitor cells (EPCs) have multiple differentiation potential and play an important role in the angiogenesis post-MI. Promoting the function of EPCs could facilitate the angiogenesis and recovery of MI. Previous studies have shown that ANGPTL3 can promote angiogenesis in corneal of rats and promote angiogenesis of endothelial cells by binding to integrin α ν β 3  receptors and promoting phosphorylation of protein kinase B (AKT). Our institution found that activated AKT can up-regulate the expression of microRNA-126 (miR-126), which can promote the proangiogenic ability of EPCs. The integrin α ν β 3  receptors and AKT also express in EPCs and are closely related to proangiogenic function. Therefore, we hypothesized that ANGPTL3 could improve function of EPCs by binding to integrin α ν β 3  receptors and up-regulating miR-126 expression via activating AKT, thus promoting the formation of new blood vessels, attenuating myocardial ischemia and improving heart function.

ANGPTL3 possibly promotes cardiac angiogenesis through improving proangiogenic ability of endothelial progenitor cells after myocardial infarction