Silencing or not silencing p63 in cardiac fibroblast, risks and benefits

Most heart diseases are often accompanied by a severe loss of cardiomyocytes (CMs) and by a pathological remodeling of the heart, culminating in heart failure or even sudden death (1). The very limited regenerative capacity of CMs is the main problem for heart repair. Cardiac reprogramming has emerged as a promising approach for cardiac regenerative therapy. Several strategies have been developed in order to get new CMs, including induced pluripotent stem cells (iPSCs) and its differentiation into CMs (2,3); activation of cardiac stem cells or stimulation of CMs to re-enter the cell cycle (4); and direct reprogramming or transdifferentiation of cardiac fibroblasts (CFs) to CMs (5,6).