Pathogenesis of atherosclerosis in diabetes mellitus.
Numerous studies have shown that patients with diabetes mellitus have accelerated atherosclerotic vascular disease, and major advances in understanding it pathogenesis have been made. Current suggestions are that endothelial injury may be the initial event in the genesis of atherosclerosis, followed by platelet adhesion and aggregation at the site of injury. In diabetes, evidence of endothelial dysfunction is present. Smooth muscle cell proliferation is an important pathologic finding in atherosclerosis. This process is stimulated by a platelet mitogen, which has been partially characterized. The mitogen has not been studied in diabetes. Lipid accumulation in the area of the atherosclerotic lesion is primarily in the form of intracellular and extracellular esterified cholesterol. In uncontrolled diabetes, elevated plasma low density lipoprotein levels and decreased plasma high density lipoprotein levels favor lipid deposition in large vessels. There is evidence of a thrombotic state in certain diabetic patients. Collectively, these abnormalities of endothelial, platelet, smooth muscle, lipoprotein, and coagulation behavior may be viewed as contributing to the problem of accelerated atherosclerosis in diabetes. A thorough understanding of the pathogenesis of this process aids in designing appropriate preventive therapeutic approaches.
D001161:Arteriosclerosis / Q000209:etiology* / Q000503:physiopathology; D001792:Blood Platelets / Q000502:physiology; D003925:Diabetic Angiopathies / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D007328:Insulin / Q000627:therapeutic use; D010974:Platelet Aggregation; D014841:von Willebrand Factor / Q000502:physiology
D007328:Insulin; D014841:von Willebrand Factor