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Despite substantial improvements in prevention, diagnosis, and therapeutic strategies, cardiovascular diseases remain the leading cause of mortality and morbidity worldwide. Cardiac fibrosis, a critical hallmark of maladaptive hypertrophy and heart failure (HF), is characterized by the excessive and uncontrolled accumulation of extracellular matrix (ECM) by cardiac fibroblasts (CFs) in the interstitial and perivascular space.1 CFs, primarily of embryonic epicardial and endothelial origins,2 are the predominant noncardiomyocyte population, accounting for 20% of total cell population in the adult murine heart.3 In addition to their traditional functions in regulating ECM synthesis and metabolism and controlling cardiac fibrosis, ECM remodeling, scar formation, and tissue repair, CFs serve as functionally pluralistic cells involved in inflammatory responses, cardiomyocyte survival, and vasculogenesis.4,5Article, see p 835 In the adult heart, CFs are present in a quiescent state with low proliferative capacity and are responsible for ECM homeostasis, providing a structural scaffold for cardiomyocytes. CFs also express gap junction protein connexin-43, which mediates electric coupling of cardiomyocytes and CFs.6 The adult mammalian heart has limited regenerative capacity after pathological injury. The repair of wounds in the heart consists of the removal of dead cardiomyocytes and replacement of myocytes loss by a collagen-based fibrotic scar to preserve myocardial integrity and cardiac function. The importance of CFs in myocardial remodeling and wound healing has been extensively studied and involves all of the 3 phases of the healing process: acute inflammatory response, proliferation, and late scar maturation. After an acute myocardial injury, CFs release proinflammatory cytokines, which promote their own proliferation in a feed-forward loop and trigger differentiation into a myofibroblast phenotype. This hyperproliferative cell type secretes high levels of proinflammatory and profibrotic factors and ECM proteins. This adaptive fibrosis can maintain structural integrity and prevent the injured heart from dysfunction and rupture; …

miR-33 Regulation of Adaptive Fibrotic Response in Cardiac Remodeling