期刊
JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH
卷 5, 期 6, 页码 837-847出版社
SPRINGER
DOI: 10.1007/s12265-012-9406-3
关键词
Fibroblast; Extracellular matrix; Cardiac remodeling; Myocardial infarction; Myofibroblast; Matricellular proteins
资金
- NIH [R01 HL-76246, HL-85440]
- Wilf Family Cardiovascular Research Institute
- Edmond J Safra/Republic National Bank of New York Chair in Cardiovascular Medicine
Cardiac fibroblasts are key cellular effectors of cardiac repair; their phenotype and function are modulated by interactions with extracellular matrix proteins. This review manuscript discusses the effects of the extracellular matrix on the inflammatory and reparative properties of fibroblasts in the infarcted myocardium. Early generation of matrix fragments in the infarct induces a pro-inflammatory and matrix-degrading fibroblast phenotype. Formation of a fibrin/fibronectin-rich provisional matrix serves as a conduit for migration of fibroblasts into the infarcted area. Induction of ED-A fibronectin and nonfibrillar collagens may contribute to myofibroblast transdifferentiation. Upregulation of matricellular proteins promotes transduction of growth factor and cytokine-mediated signals. As the scar matures, matrix cross-linking, clearance of matricellular proteins, and reduced growth factor signaling cause deactivation and apoptosis of reparative infarct fibroblasts. Understanding the effects of matrix components on infarct fibroblasts may guide the design of peptides that reproduce, or inhibit, specific matricellular functions, attenuating adverse remodeling.
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