Collagen synthesis in atherosclerosis: too much and not enough.
Fibrillar collagen is a critical component of atherosclerotic lesions. Uncontrolled collagen accumulation leads to arterial stenosis, while excessive collagen breakdown combined with inadequate synthesis weakens plaques thereby making them prone to rupture. This review discusses cellular sources of collagen synthesis in atherosclerosis, local and systemic factors modulating collagen gene expression, as well as temporal and spatial patterns of collagen production in human and experimental atherosclerotic lesions.
Rekhter
M D
MD
Department of Cardiovascular Therapeutics, Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, Ann Arbor, MI 48105, USA. mark.rekhter@wl.com
D001158:Arteries / Q000378:metabolism; D001161:Arteriosclerosis / Q000378:metabolism*; D003094:Collagen / Q000096:biosynthesis*; D004730:Endothelium, Vascular / Q000378:metabolism; D006710:Homocysteine / Q000378:metabolism; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*
D006710:Homocysteine; D003094:Collagen