TY - JOUR
T1 - Cardiac fibrosis
T2 - The fibroblast awakens
AU - Travers, Joshua G.
AU - Kamal, Fadia A.
AU - Robbins, Jeffrey
AU - Yutzey, Katherine E.
AU - Blaxall, Burns C.
N1 - Funding Information:
We wish to acknowledge Jeffery Molkentin for his astute suggestions during the development of this review. This work was supported by National Institutes of Health grants R01 HL091475, R01 HL129772, R01 HL132551, R01 GM097347, U54 HL119810 (B.C. Blaxall), and P01 HL069779 (B.C. Blaxall, J. Robbins, and K.E. Yutzey), an American Heart Association Postdoctoral Fellowship (F.A. Kamal), and a Predoctoral Fellowship from the Pharmaceutical Research and Manufacturers of America Foundation (J.G. Travers).
Publisher Copyright:
© 2016 American Heart Association, Inc.
PY - 2016/3/18
Y1 - 2016/3/18
N2 - 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.
AB - 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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U2 - 10.1161/CIRCRESAHA.115.306565
DO - 10.1161/CIRCRESAHA.115.306565
M3 - Review article
C2 - 26987915
AN - SCOPUS:84961778300
SN - 0009-7330
VL - 118
SP - 1021
EP - 1040
JO - Circulation research
JF - Circulation research
IS - 6
ER -
