Albert Einstein College of Medicine Bronx United States
Heart fibrosis and loss of blood vessels are prominent pathologic abnormalities in diabetics that lead to the development ofheart failure. Moreover, reduced angiogenesis after a heart attack is responsible for defective myocardial repair in diabeticsubjects. Although the negative impact of diabetes on the heart is widely appreciated, the cellular alterations and molecularsignals involved in fibrosis and blood vessel loss in diabetes remain unknown. Applying genetic fate mapping tools, we haveuncovered an unexpected plasticity and heterogeneity in reparative cells and identified common cellular links betweenangiogenesis and fibrosis. We investigate the role of these novel biological mechanisms in the pro-fibrotic and angiostaticeffects of diabetes, focusing on the contribution of pericytes and endothelial cells in the cardiac tissue repair process.