Chemokines and cardiac fibrosis

Research output: Contribution to journalArticle

64 Scopus citations

Abstract

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

Keywords

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

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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