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

Marcin Dobaczewski, Judith J. De Haan, Nikolaos G. Frangogiannis

Research output: Contribution to journalArticlepeer-review

82 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)837-847
Number of pages11
JournalJournal of Cardiovascular Translational Research
Issue number6
StatePublished - Dec 2012


  • Cardiac remodeling
  • Extracellular matrix
  • Fibroblast
  • Matricellular proteins
  • Myocardial infarction
  • Myofibroblast

ASJC Scopus subject areas

  • Molecular Medicine
  • Genetics
  • Pharmaceutical Science
  • Cardiology and Cardiovascular Medicine
  • Genetics(clinical)


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