Proliferation and directed migration of vascular cells are key components in fibroproliferative vascular diseases such as atherosclerosis and restenosis following percutaneous transluminal coronary angioplasty (PTCA). However, the precise cellular and molecular mechanisms involved in the control of vascular cell proliferation or migration at the tissue level remain largely undefined. Molecules contributing to these processes are elaborated by distinct cell types and act in both autocrine and paracrine modes. They include two broad classes, polypeptide growth factors and vasoactive G-protein-coupled receptor (GPCR) agonists. Examples of the former, such as platelet-derived growth factor (PDGF), bind to and activate cell surface receptor tyrosine kinases, initiating intracellular biochemical signaling pathways associated with cell proliferation or migration. In contrast, recent evidence suggests that vasoactive GPCR agonists [e.g, angiotensin II (All), endothelin-l (ET-I), athrombin] elicit cell growth indirectly by inducing the production of autocrine or paracrine factors in vascular cells. This review summarizes recent studies on the cellular and molecular mechanisms involved in vascular smooth muscle cell growth control as well as provides information on possible therapeutic targets in this active area of vascular biological research.
|Original language||English (US)|
|Number of pages||12|
|Journal||Current Pharmaceutical Design|
|State||Published - Dec 1 1997|
All Science Journal Classification (ASJC) codes
- Drug Discovery