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.
Mitropoulos
K A
KA
Medical Research Council Epidemiology and Medical Care Unit, Wolfson Institute of Preventive Medicine, Medical College of St Bartholomew's Hospital, London, UK.
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