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      Cardiac Fibrosis: The Fibroblast Awakens.

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          Abstract

          Myocardial fibrosis is a significant global health problem associated with nearly all forms of heart disease. Cardiac fibroblasts comprise an essential cell type in the heart that is responsible for the homeostasis of the extracellular matrix; however, upon injury, these cells transform to a myofibroblast phenotype and contribute to cardiac fibrosis. This remodeling involves pathological changes that include chamber dilation, cardiomyocyte hypertrophy and apoptosis, and ultimately leads to the progression to heart failure. Despite the critical importance of fibrosis in cardiovascular disease, our limited understanding of the cardiac fibroblast impedes the development of potential therapies that effectively target this cell type and its pathological contribution to disease progression. This review summarizes current knowledge regarding the origins and roles of fibroblasts, mediators and signaling pathways known to influence fibroblast function after myocardial injury, as well as novel therapeutic strategies under investigation to attenuate cardiac fibrosis.

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          Author and article information

          Journal
          Circ. Res.
          Circulation research
          1524-4571
          0009-7330
          Mar 18 2016
          : 118
          : 6
          Affiliations
          [1 ] From the Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, OH.
          [2 ] From the Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, OH. Burns.Blaxall@cchmc.org.
          Article
          CIRCRESAHA.115.306565 NIHMS762596
          10.1161/CIRCRESAHA.115.306565
          26987915
          © 2016 American Heart Association, Inc.

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