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 language | English (US) |
|---|---|
| Pages (from-to) | 101-107 |
| Number of pages | 7 |
| Journal | Inflammation and Allergy - Drug Targets |
| Volume | 6 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jun 2007 |
| Externally published | Yes |
Keywords
- Cardiomyopathy
- Chemokine
- Cytokine
- Fibrosis
- Infarction
- Inflammation
- MCP-1
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Pharmacology