Apoptosis of vascular smooth muscle cells in vascular remodelling and atherosclerotic plaque rupture.
Apoptosis (programmed cell death) of vascular smooth muscle cells (VSMCs) has recently been identified as an important process in a variety of human vascular diseases, including atherosclerosis, arterial injury, and restenosis after angioplasty. VSMC apoptosis is regulated by interactions between the local cell-cell and cytokine environment within the arterial wall, and the expression of pro- and anti-apoptotic proteins by the cell, including death receptors, proto-oncogenes and tumour suppressor genes. This review summarises our current knowledge of the occurrence and mechanisms underlying VSMC apoptosis in atherosclerosis and arterial remodelling.
Bennett
M R
MR
British Heart Foundation Sr. Fellow, Addenbrooke's Hospital, Department of Medicine, Cambridge, UK. mrb@mole.bio.cam.ac.uk
D000818:Animals; D017209:Apoptosis; D001158:Arteries / Q000378:metabolism / Q000473:pathology; D001161:Arteriosclerosis / Q000378:metabolism / Q000473:pathology*; D005109:Extracellular Matrix / Q000378:metabolism; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism; D008666:Metalloendopeptidases / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D009569:Nitric Oxide / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism
D008077:Lipoproteins, LDL; D019253:Proto-Oncogene Proteins c-bcl-2; D009569:Nitric Oxide; D008666:Metalloendopeptidases