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Cardiac Fibroblast GRK 2 Deletion Enhances Contractility and Remodeling Following Ischemia / Reperfusion Injury

Cardiac fibroblasts represent the largest population of interstitial cells in myocardium. They are responsible for secreting and maintaining the extracellular matrix forming a 3-dimensional scaffold supporting the surrounding myocytes. Although not contractile, fibroblasts are directly connected to myocytes through cell junctions and may act as bridges to connect myocytes electrically isolated by connective tissue. Unlike myocytes, cardiac fibroblasts are particularly resistant to hypoxia and so play multiple roles in the cascade of events after ischemic injury. After ischemic injury, cardiac fibroblasts transform into a specialized cell type called a myofibroblast marked by increased amounts of α-smooth muscle actin (α-SMA) and characterized as being hyper-secretory. Myofibroblasts have a critical role in cardiac remodeling by forming a collagen-rich scar that allows the infarcted area to maintain structural integrity after cardiomyocyte death. Additionally, in response to injury, fibroblasts secrete cytokines and chemokines that have important roles in the immediate inflammatory stage. Fibroblasts are responsive to a variety of stimuli for these above functions, including agents that activate membrane-bound G protein– coupled receptors (GPCRs). Thus, regulation of these receptors is important in the overall process of myofibroblast activation after injury.