MCP-1/CCL2 as a therapeutic target in myocardial infarction and ischemic cardiomyopathy.
MCP-1/CCL2 as a therapeutic target in myocardial infarction and ischemic cardiomyopathy.
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DOI：
10.2174/187152807780832265
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发表时间：
2007-05
期刊：
影响因子：
--
通讯作者：
Ying Xia;N. Frangogiannis
中科院分区：
文献类型：
--
作者：
Ying Xia;N. Frangogiannis
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.
