Chemokines and cardiac fibrosis

Research output: Contribution to journalArticlepeer-review

88 Scopus citations


Several members of the chemokine family play an important role in reparative fibrosis and are involved in the pathogenesis of remodeling following myocardial infarction. Chemokines may regulate the fibrotic process through recruitment and activation of mononuclear cell subsets and fibroblast progenitors (fibrocytes), by exerting direct effects on resident fibroblasts, and by modulating angiogenesis. Monocyte Chemoattractant Protein (MCP)-1/CCL2 is the best studied chemokine in cardiac fibrosis. Disruption of the MCP-1 axis reduces fibrosis attenuating dilation of the infarcted ventricle. In addition, MCP-1 signaling is activated in response to insults that do not cause cardiomyocyte death, such as brief ischemia or pressure overload and regulates fibrous tissue deposition in experimental models of fibrotic non-infarctive cardiomyopathy. Understanding the role of chemokinemediated interactions in the development of cardiac fibrosis may identify novel therapeutic targets for treatment of patients with heart failure.

Original languageEnglish (US)
Pages (from-to)391-405
Number of pages15
JournalFrontiers in Bioscience - Scholar
Volume1 S
Issue number2
StatePublished - Jan 6 2009
Externally publishedYes


  • Cardiac fibrosis
  • Cardiomyopathy
  • Chemokines
  • Extracellular matrix
  • Heart failure
  • MCP-1
  • MIP-1alpha
  • Myocardial infarction
  • Myofibroblast
  • TGF-beta

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology
  • General Immunology and Microbiology


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