Abstract
The cardiac extracellular matrix (ECM) is critical for maintaining cardiac shape and function. Disruption of the ECM network and dysregulation of matrix homeostasis and metabolism result in adverse cardiac remodeling with shape deformation and dysfunction that leads to heart failure (HF), disability and death. A key mechanism in the development and progression of HF due to injury caused by myocardial infarction and hypertension, the two leading causes of HF, involves adverse cardiac ECM remodeling, which participates in the march to end-stage HF. Improved therapeutic strategies that include targeting of adverse cardiac ECM remodeling could prevent, limit or reverse progression to HF.
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