Key result
Cardiac fibroblasts are a major source of matrix metalloproteinases in the heart, representing a viable therapeutic target for regulating extracellular matrix turnover in cardiac pathologies.
Cardiac fibroblasts are a major source of matrix metalloproteinases in the heart, making them a viable therapeutic target for mitigating adverse myocardial remodeling in various cardiac pathologies.
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May support fibroblast modulation to curb adverse remodeling; leaves open targeted inhibitor development and clinical validation.
Cardiac fibroblasts (CF) play a key role in orchestrating the structural remodeling of the myocardium in response to injury or stress, in part through direct regulation of extracellular matrix (ECM) turnover. The matrix metalloproteinases (MMPs) are a family of over 25 zinc-dependent proteases that together have the capacity to degrade all the protein components of the ECM. Fibroblasts are a major source of several MMPs in the heart, thereby representing a viable therapeutic target for regulating ECM turnover in cardiac pathologies characterized by adverse remodeling, such as myocardial infarction, cardiomyopathy, hypertension and heart failure. This review summarizes current knowledge on the identity and regulation of MMPs expressed by CF and discusses future directions for reducing adverse myocardial remodeling by modulating the expression and/or activity of CF-derived MMPs.
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Turner et al. (2012) conducted a review in Adverse myocardial remodeling. Modulation of cardiac fibroblast-derived matrix metalloproteinases was evaluated. Cardiac fibroblasts are a major source of matrix metalloproteinases in the heart, representing a viable therapeutic target for regulating extracellular matrix turnover in cardiac pathologies.
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