Fig. 1

Mechanisms of action of MSCs for cardiac regeneration. (a) miR-133a downregulates the expression of Apaf-1 and caspase 3 and 9, leading to attenuated fibrosis. ECs producing growth factors such as VEGF-A help in recruiting the peripheral stem cells, along with coordinating the differentiation of MSCs into endothelial cells, thereby leading to vascularization. BMP7 expressed by MSCs lead to inhibition of fibrosis on counteraction of TGF-β secreted by macrophages. 5-azacytidine induces differentiation of MSCs into cardiomyocyte, thereby mitigating cardiac contractibility. (b) PLGF-induced macrophage polarization from M1 to M2 promotes neovascularization. CardioChimeras are mono-nucleate fusion of CSCs and MSCs which have exclusive growth kinetics, and have proven to be superior to the parent precursors. (c) MSCs pretreated with various compounds show cryoprotective effects along with enhanced cardiomyogenesis and improved heart function.  bFGF basic fibroblast growth factor, CSC cardiac stem cell, EC endothelial cell, HGF hepatocyte growth factor, LV left ventricular, MSC mesenchymal stem cell, PLGF platelet-derived growth factor, TGF tumor growth factor, VCAM vascular cell adhesion molecule, VEGF vascular endothelial growth factor