According to the World Health Organization, cardiovascular diseases are the major cause of death worldwide, representing 32% of all global death, 85% of which are due to heart attack and stroke. During myocardial infarction a large number of cells die within the area subjected to ischemia, in the first 6 to 24 hours. However, heart has a very limited self-regeneration capacity leading to a permanent loss of cardiomyocytes in the site of the ischemic event. Moreover, fibroblasts change their phenotype into myofibroblasts, leading to increased collagen deposition, tissue stiffening and consequent heart failure. Conventional pharmaceutical therapies target mechanisms against maladaptive regulators activated by left ventricular dysfunction, such as inhibitors of the renin-angiotensin system, the mineralocorticoid receptor, the sympathetic nervous system and, more recently, the natriuretic system.