作者: Motoji Sawabe
DOI: 10.1111/J.1447-0594.2010.00603.X
关键词: Pathology 、 Artery 、 Left ventricular hypertrophy 、 Glycation 、 Elastin 、 Endothelial dysfunction 、 Anatomy 、 Medicine 、 Endothelium 、 Aortic aneurysm 、 Pathogenesis
摘要: The large and medium-sized arteries in elderly people show varying degrees of intimal medial change. change is known as age-related degeneration sclerosis (ARMDS). ARMDS results systolic hypertension left ventricular hypertrophy the heart a result loss arterial elasticity. It also causes aortic dilatation, or even aneurysm. atherosclerosis are distinct entities, but often overlapped confused with each other. present review mainly focuses on briefly addresses atherosclerosis, aging arterioles, capillaries veins. smooth muscle cells inner half media degenerate undergo apoptosis. This degradation elastin fibers accumulation collagen media, inflammatory infiltrates scarce. Biochemical studies showed an decrease its crosslinks, increase crosslink. Because turnover very long, it likely suffers from glycation (Maillard reaction) glyco-oxidative reaction. advanced end-products accumulate increasing age. Alcian-blue positive mucin accumulates people. major component chondroitin-6-sulfate. Microcalcification frequent acellular portion Calcium contents In conclusion, pathological entity clinical significance. pathogenesis unclear; mechanical stress elastin, endothelial dysfunction, proposed. Geriatr Gerontol Int 2010; 10 (Suppl. 1): S213–S220.