MCP-1/CCL2 as a Therapeutic Target in Myocardial Infarction and Ischemic Cardiomyopathy

Author(s): Ying Xia, Nikolaos G. Frangogiannis

Journal Name: Inflammation & Allergy - Drug Targets (Discontinued)
Formerly Current Drug Targets - Inflammation & Allergy

Volume 6 , Issue 2 , 2007


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.

Keywords: Inflammation, infarction, chemokine, MCP-1, cytokine, cardiomyopathy, fibrosis

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Article Details

Year: 2007
Page: [101 - 107]
Pages: 7
DOI: 10.2174/187152807780832265
Price: $65

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