Abstract
The failing heart is subject to alterations in loading pressures and hemodynamic strain. A characteristic pathological finding in heart failure is increased interstitial fibrosis and global ventricular remodeling with concomitant alterations in extracellular matrix (ECM) composition. The dynamic response of myocytes to changes in mechanical strain leads to alterations in coupling and paracrine signaling between these cells and interstitial fibroblasts.
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