Cyclic Strain and Interstitial Flow Modulate Cardiac Fibroblast Phenotype Through Angiotensin II and TGF-β Pathways

A fibrotic scar in the myocardium is characterized by excessive extracellular matrix deposition, loss of functioning cardiomyocytes, and the transition of healthy cardiac fibroblasts to a myofibroblast phenotype. Previous research has suggested that the myofibroblast transition is mediated by mechanical stimuli including cyclic strain [1–2] and interstitial fluid flow [3–5].