MCP-1/CCL2 as a therapeutic target in myocardial infarction and ischemic cardiomyopathy

Research output: Contribution to journalReview articlepeer-review

52 Scopus citations

Abstract

The CC chemokine Monocyte Chemoattractant Protein (MCP)-1/CCL2 mediates recruitment of mononuclear cells, modulates monocyte and lymphocyte phenotype and regulates fibrous tissue deposition and angiogenesis. MCP-1 is markedly induced in the infarcted myocardium and plays an important role in infarct healing and post-infarction remodeling. MCP-1 null mice exhibit decreased macrophage recruitment in the infarcted heart, delayed phagocytosis of dead cardiomyocytes, diminished fibroblast infiltration and attenuated left ventricular remodeling. Targeted deletion of CCR2, the primary MCP-1 receptor also protects from the development of adverse remodeling following myocardial infarction. In addition to its role in infarct healing, MCP-1 signaling plays an important role in the development of interstitial fibrosis in a mouse model of brief repetitive myocardial ischemia and reperfusion. Our review manuscript discusses the mechanisms responsible for MCP-1-mediated effects in the ischemic myocardium and explores MCP-1 targeting as a novel therapeutic approach in patients with myocardial infarction and ischemic non-infarctive cardiomyopathy.

Original languageEnglish (US)
Pages (from-to)101-107
Number of pages7
JournalInflammation and Allergy - Drug Targets
Volume6
Issue number2
DOIs
StatePublished - Jun 2007
Externally publishedYes

Keywords

  • Cardiomyopathy
  • Chemokine
  • Cytokine
  • Fibrosis
  • Infarction
  • Inflammation
  • MCP-1

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pharmacology

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