Lipoprotein metabolism and thrombosis.
Recent evidence suggests that long-chain saturated fatty acids (i.e. stearic acid), produced on lipolysis of triglyceride-rich lipoproteins in the interface of circulating remnant particles provide a contact surface that activates the contact system of coagulation and subsequently activates factor VII. Increased level of circulating activated factor VII is probably of little consequence to a healthy individual with minimal expression of tissue factor in the vasculature. However, at a site of an atheromatous plaque or at a vascular injury site where there is tissue factor activity, increased circulating activated factor VII is expected to generate thrombin at a higher rate. Propagation of the prothrombotic environment will be facilitated on expression of additional tissue factor that is induced by the local increased concentration of thrombin. Thrombin with its receptor-mediated interactions with blood and vessel wall cells can signal inflammatory and proliferative responses such as those that occur in atheroma.
Medical Research Council Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, Medical College of St Bartholomew's Hospital, London, UK.
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Mitropoulos
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000378:metabolism*; D001777:Blood Coagulation / Q000502:physiology*; D001798:Blood Proteins / Q000502:physiology; D005167:Factor VII / Q000378:metabolism; D006801:Humans; D008074:Lipoproteins / Q000378:metabolism*; D013917:Thrombin / Q000096:biosynthesis; D013925:Thromboplastin / Q000096:biosynthesis; D013927:Thrombosis / Q000209:etiology / Q000378:metabolism*
D001798:Blood Proteins; D008074:Lipoproteins; D005167:Factor VII; D013925:Thromboplastin; D013917:Thrombin