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Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling

Discovery & Translational Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine (LICAMM), School of Medicine, University of Leeds, Leeds LS2 9JT, UK
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J. Cardiovasc. Dev. Dis. 2019, 6(3), 27; https://doi.org/10.3390/jcdd6030027
Received: 23 July 2019 / Revised: 2 August 2019 / Accepted: 6 August 2019 / Published: 7 August 2019
(This article belongs to the Special Issue Cardiac Fibroblasts and Fibrosis)
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Abstract

The cardiac fibroblast is a remarkably versatile cell type that coordinates inflammatory, fibrotic and hypertrophic responses in the heart through a complex array of intracellular and intercellular signaling mechanisms. One important signaling node that has been identified involves p38 MAPK; a family of kinases activated in response to stress and inflammatory stimuli that modulates multiple aspects of cardiac fibroblast function, including inflammatory responses, myofibroblast differentiation, extracellular matrix turnover and the paracrine induction of cardiomyocyte hypertrophy. This review explores the emerging importance of the p38 MAPK pathway in cardiac fibroblasts, describes the molecular mechanisms by which it regulates the expression of key genes, and highlights its potential as a therapeutic target for reducing adverse myocardial remodeling.
Keywords: cardiac remodeling; extracellular matrix; fibroblast; fibrosis; heart; hypertrophy; inflammation; myofibroblast; p38 MAP kinase; signal transduction; stress-activated protein kinase; transcription factor cardiac remodeling; extracellular matrix; fibroblast; fibrosis; heart; hypertrophy; inflammation; myofibroblast; p38 MAP kinase; signal transduction; stress-activated protein kinase; transcription factor
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Turner, N.A.; Blythe, N.M. Cardiac Fibroblast p38 MAPK: A Critical Regulator of Myocardial Remodeling. J. Cardiovasc. Dev. Dis. 2019, 6, 27.

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