Journal
CELLULAR SIGNALLING
Volume 19, Issue 7, Pages 1359-1371Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2007.03.002
Keywords
intimal hyperplasia; vascular remodeling; angioplasty; signaling; coronary artery bypass graft; smooth muscle cells; endothelial cells; endothelium; extracellular-regulated kinases; ERK; JNK; p38MAPK; FGF; TGF; MMP; thrombin; inflammation; topical inhibition; restenosis; percutaneous coronary intervention; growth factors
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Funding
- NHLBI NIH HHS [5R01 HL 70203-01] Funding Source: Medline
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Cardiovascular interventions that restore blood circulation to ischemic areas are accompanied by significant tissue damage, which triggers a vascular remodeling response that may result in restenosis of blood conduits. Early endothelial dysfunction and/or impairment is the early event of a cascade that leads, through an inflammatory response and dedifferentiation of medial smooth muscle cells with abundant deposition of extracellular matrix, to intimal hyperplasia. Here we present the molecular and cellular mechanisms of intimal hyperplasia secondary to vascular injury and discuss the potential role of therapeutic modulation of the intracellular signaling pathways that differentially effect vascular endothelial and smooth muscle cells. The role of mitogen-activated protein kinases (MAPKs) and the outcome of their modulation in these processes are highlighted here as they provide a promising therapeutic target for prevention of restenosis. (c) 2007 Elsevier Inc. All rights reserved.
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