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Cardiac fibroblasts: from development to heart failure

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Abstract

Cardiac fibroblasts are a major cell population of the heart and are characterized by their capacity to produce extracellular matrix (ECM). In hearts subjected to pressure overload, excessive fibroblast accumulation is responsible for fibrosis of the myocardium, a major clinical issue. Hence, understanding mechanisms generating fibroblasts in this context has become a key question in the cardiovascular field. Recent studies now point to the activation of resident fibroblasts as the underlying cause of fibrosis. However, de novo generation of fibroblasts from endothelium and circulating hematopoietic cells has also been proposed to significantly contribute to fibrosis. Here, we discuss the latest findings on fibroblast origins, with a particular emphasis on the pressure overload model, and the implication of these findings for the development of anti-fibrotic therapies that are currently lacking.

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Acknowledgments

T. Moore-Morris is funded by WHRI-COFUND, the Leducq Foundation, and the Lefoulon-Delalande foundation. KE Yutzey is funded by NIH/NHLBI P01HL069779. M. Puceat would like to acknowledge funding from the Leducq Foundation. SM. Evans is funded by grants from the National Heart, Lung, and Blood Institute.

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Correspondence to Sylvia M. Evans.

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Moore-Morris, T., Guimarães-Camboa, N., Yutzey, K.E. et al. Cardiac fibroblasts: from development to heart failure. J Mol Med 93, 823–830 (2015). https://doi.org/10.1007/s00109-015-1314-y

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