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.
Highlights
Once viewed as relatively passive players that solely regulate extracellular matrix (ECM) remodeling, cardiac fibroblasts are acknowledged as being the primary nodal regulators of multiple aspects of cardiac function under both physiological and pathophysiological conditions [1,2,3,4]
In addition to modulating ECM turnover, cardiac fibroblasts contribute to cardiac inflammation, angiogenesis and cardiomyocyte hypertrophy, and are viewed as an important potential therapeutic target for ameliorating adverse cardiac remodeling [5]
The aim of this review is to discuss the importance of p38 Mitogen-activated protein kinase (MAPK) in regulating cardiac fibroblast function in the context of cardiac remodeling, to describe the underlying molecular mechanisms, and to highlight the value of cardiac fibroblast p38 signaling as a potential therapeutic target
Summary
Once viewed as relatively passive players that solely regulate extracellular matrix (ECM) remodeling, cardiac fibroblasts are acknowledged as being the primary nodal regulators of multiple aspects of cardiac function under both physiological and pathophysiological conditions [1,2,3,4]. Mitogen-activated protein kinase (MAPK) intracellular signaling pathways are central regulators of multiple aspects of cellular function in all tissues, including the heart [6]. The aim of this review is to discuss the importance of p38 MAPK in regulating cardiac fibroblast function in the context of cardiac remodeling, to describe the underlying molecular mechanisms, and to highlight the value of cardiac fibroblast p38 signaling as a potential therapeutic target
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