Proliferation, migration, matrix turnover, and death of smooth muscle cells in native coronary and vein graft atherosclerosis.
Smooth muscle cells migrate into the vascular intima, proliferate, and lay down extracellular matrix, thereby forming an important component of the occlusive mass of atherosclerotic plaques in native arteries and in saphenous vein grafts. The viability of smooth muscle cells and the integrity of their surrounding extracellular matrix also determine the liability of plaques to rupture and hence precipitate myocardial infarction and vein graft occlusion. This update reviews recent developments in the molecular understanding of relevant aspects of smooth muscle cell biology. It highlights the increasing importance attached to interactions between growth factors and components of the extracellular matrix in regulating migration and proliferation and the new roles assigned to apoptosis in these cells. It illustrates, furthermore, how the application of the techniques of molecular biology is identifying new targets for conventional and gene therapy.
Newby
A C
AC
Bristol Heart Institute, Bristol Royal Infirmary, UK.
George
S J
SJ
D000818:Animals; D017209:Apoptosis; D002455:Cell Division; D002465:Cell Movement; D003324:Coronary Artery Disease / Q000473:pathology*; D005109:Extracellular Matrix / Q000378:metabolism; D006801:Humans; D008666:Metalloendopeptidases / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000473:pathology*; D010982:Platelet-Derived Growth Factor / Q000502:physiology; D012501:Saphenous Vein / Q000473:pathology* / Q000637:transplantation*; D016212:Transforming Growth Factor beta / Q000502:physiology
D010982:Platelet-Derived Growth Factor; D016212:Transforming Growth Factor beta; D008666:Metalloendopeptidases