Fibrinogen and atherosclerosis.
Fibrin appears to be a multi-potential component of atherogenesis, intervening at virtually all stages of lesion development. Fibrin and microthrombus deposition on normal intima is associated with endothelial disruption and intimal oedema, and oedema is a primary characteristic of early proliferative lesions. Fibrin strands on or in the intima encourage smooth muscle cell (SMC) migration and proliferation, and contribute to the growth of plaques. Fibrin also provides a continuing source of fibrin degradation products (FDP), and these have mitogenic activity which will sustain SMC proliferation in growing plaques, and act as chemoattractants for blood leucocytes. Accumulation of the lipid core in fibrous plaques may also be influenced by fibrin which appears to bind the lipoprotein Lp(a) with high affinity, thereby immobilizing its lipid moiety within the lesion.
Smith
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Department of Clinical Biochemistry, Medical School, Aberdeen Royal Infirmary, U.K.
D001161:Arteriosclerosis / Q000097:blood* / Q000473:pathology; D001798:Blood Proteins / Q000378:metabolism; D002455:Cell Division / Q000502:physiology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005340:Fibrinogen / Q000378:metabolism*; D005352:Fibromuscular Dysplasia / Q000097:blood / Q000473:pathology; D006801:Humans; D008055:Lipids / Q000097:blood; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology
D001798:Blood Proteins; D008055:Lipids; D005340:Fibrinogen