Vascular injury and modulation of MAPKs: a targeted approach to therapy of restenosis.
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.
Yu
Pey-Jen
PJ
The Seymour Cohn Cardiovascular Research Laboratory, Department of Cardiothoracic Surgery, New York University School of Medicine, New York, NY 10016, USA.
Ferrari
Giovanni
G
Pirelli
Luigi
L
Gulkarov
Iosif
I
Galloway
Aubrey C
AC
Mignatti
Paolo
P
Pintucci
Giuseppe
G
D000818:Animals; D023903:Coronary Restenosis / Q000201:enzymology* / Q000628:therapy*; D006133:Growth Substances / Q000378:metabolism; D006801:Humans; D006965:Hyperplasia; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D017539:Tunica Intima / Q000473:pathology
D006133:Growth Substances; D020928:Mitogen-Activated Protein Kinases