Elucidating the periostin-mediated dynamics in biological and pathological processes of cardiac fibroblasts within cardiac fibrosis

Heart disease continues to be the number one killer in the United States accounting for 1 in every 9 deaths. Furthermore, over 6 million people are currently living with heart failure in the US, costing 30 billion dollars each year. In essence, heart disease develops because the cardiac tissue, unlike skeletal muscle or skin, lacks a robust regenerative capacity. Thus, an ischemic injury to the heart almost always results in a permanent loss of cardiac myocytes, inducing a cascade of pathological responses that result in interstitial fibrosis, loss of ventricular compliance, and chamber remodeling. For years, development of new therapies to cure heart failure has primarily focused on the repair and replacement of cardiomyocytes since they constitute most of the heart by volume and are the fundamental contractile cells that generate the force to pump blood to the body. However, more and more studies are now showing the importance of noncardiomyocytes and their interactions with cardiomyocytes in maintaining cardiac homeostasis during health and disease. In fact, recent calculations show that cardiomyocytes account for only 30% of the total cell count in the adult mouse with the majority represented by supportive cell populations such as endothelial cells, hematopoietic-derived cells, fibroblasts, and smooth muscle cells. This new avenue of non-cardiomyocyte biology is at the forefront of the efforts in developing new therapies to treat heart disease which requires extensive research to decipher the relevance and the role of these non-myocyte populations in homeostasis, disease, and injury to the heart.