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作 者:丁玲 于菲[1] 荆红运 关秀茹[1] Ding Ling;Yu Fei;Jing Hongyun;Guan Xiuru(Department of Laboratory Diagnostics,the First Affiliated Hospital of Harbin Medical University,Harbin 150001,China)
机构地区:[1]哈尔滨医科大学附属第一医院检验科,150001
出 处:《国际免疫学杂志》2018年第5期570-573,共4页International Journal of Immunology
基 金:国家自然科学基金(81672084)。
摘 要:动脉粥样硬化(atherosclerosis,AS)导致的冠心病、脑卒中及外周动脉疾病等是人类致残、致死的主要原因。目前研究发现,正常情况下适度的自噬可以通过防止内皮细胞损伤、抑制平滑肌细胞异常增殖以及防止巨噬细胞泡沫化来延缓As的发生及发展。但晚期过度的自噬则会加重内皮细胞炎症,导致平滑肌细胞坏死从而加剧As斑块的不稳定性。因此深入讨论As与自噬的关系及其相关机制可以为砖的防治提供新的靶点。The main causes of human disability and death include coronary heart disease,stroke,and peripheral arterial disease,which are caused by atherosclerosis(AS).Studies found that moderate autophagy in healthy condition can delay the occurrence and development of AS by preventing endothelial cell injury,inhibiting the abnormal proliferation of smooth muscle cells,and preventing the foaming of maerophages.However,excessive autophagy could aggravate the endothelial cell inflammation and induce smooth muscle cell necrosis, which aggravates the instability of atheroselerofic plaque in advanced AS.Therefore,to understand the relation-ship between AS and autophagy may provide new targets for the prevention and treatment of AS.
分 类 号:R543.5[医药卫生—心血管疾病]
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