The extracellular matrix modulates fibroblast phenotype and function in the infarcted myocardium.

摘要: Cardiac fibroblasts are key cellular effectors of cardiac repair; their phenotype and function modulated by interactions with extracellular matrix proteins. This review manuscript discusses the effects on inflammatory reparative properties in infarcted myocardium. Early generation fragments infarct induces a pro-inflammatory matrix-degrading fibroblast phenotype. Formation fibrin/fibronectin-rich provisional serves as conduit for migration into area. Induction ED-A fibronectin nonfibrillar collagens may contribute to myofibroblast transdifferentiation. Upregulation matricellular proteins promotes transduction growth factor cytokine-mediated signals. As scar matures, cross-linking, clearance proteins, reduced signaling cause deactivation apoptosis fibroblasts. Understanding components guide design peptides that reproduce, or inhibit, specific functions, attenuating adverse remodeling.