Cardiac fibroblasts become activated following injury and participate in repair and remodeling of the heart.
The authors discuss the phenotypic alterations and role of fibroblasts in infarcted and failing hearts.
In failing hearts, fibroblasts may deposit ECM proteins, increasing myocardial stiffness, but may also exert protective and reparative actions.
Future studies will focus on characterization of the phenotypic heterogeneity of cardiac fibroblasts that may explain their functional diversity.
Expansion and activation of fibroblasts following cardiac injury is important for repair but may also contribute to fibrosis, remodeling, and dysfunction. The authors discuss the dynamic alterations of fibroblasts in failing and remodeling myocardium. Emerging concepts suggest that fibroblasts are not unidimensional cells that act exclusively by secreting extracellular matrix proteins, thus promoting fibrosis and diastolic dysfunction. In addition to their involvement in extracellular matrix expansion, activated fibroblasts may also exert protective actions, preserving the cardiac extracellular matrix, transducing survival signals to cardiomyocytes, and regulating inflammation and angiogenesis. The functional diversity of cardiac fibroblasts may reflect their phenotypic heterogeneity.