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热休克蛋白90调节内皮一氧化氮合酶(一个新近认识的心血管疾病调节物)(英文) 被引量：2

Regulation of Endothelial Nitric Oxide Synthase by Heat Shock Protein 90 (A Newly Recognized Player in Cardiovascular Diseases)
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摘要 阐述热休克蛋白90(hsp90)作为一个心血管疾病新的调节物,在调节内皮一氧化氮合酶(eNOS)功能方面的作用:血管内皮一氧化氮(NO)主要来源于eNOS;eNOS同时有产生NO和氧阴离子自由基()的功能。NO与的平衡在调节心血管方面有着重要的作用,当这个平衡被打破时可导致多种心血管疾病的发生发展;实验发现,当hsp90与eNOS结合增加时,eNOS耦联产生NO,当hsp90与eNOS结合减少或结合后无发生结构改变时eNOS非耦联产生。进而提出深入探讨hsp90调节eNOS机制的必要性。-.O2-.O2-. The aim of this article was to illustrate the effect of regulation of endothelial nitric oxide synthase (eNOS) by heat shock protein 90 (hsp90), a newly recognized player in cardiovascular diseases. eNOS is the major source of nitric oxide (NO) in vascular endothelial cells. eNOS has two activities, producing NO and generating superoxide anion ( ). The balance between NO and may play important roles in regulating cardiovascular system. Disturbances in this balance may lead to many cardiovascular diseases. When increase of hsp90 associated with eNOS, eNOS couples and generates NO, when decrease of hsp90 associated with eNOS or no changes on hsp90 conformation after associated with eNOS, eNOS uncouples and generates . It is necessary to understand how hsp90 regulates eNOS in the future.
作者 区景松 Kirkwood A.PRITCHARD Jr
机构地区 广州医学院第一附属医院广州呼吸疾病研究所心胸外科 Division of Pediatric Surgery
出处 《中山大学学报（医学科学版）》 CAS CSCD 北大核心 2004年第6期493-495,503,共4页 Journal of Sun Yat-Sen University:Medical Sciences
关键词 热休克蛋白90 内皮一氧化氮合酶 心血管疾病 调节物 ENOS heat shock protein 90 nitric oxide synthase nitric oxide superoxide endothelial cell
分类号 R54 [医药卫生—心血管疾病] R977.3 [医药卫生—药品]
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参考文献19

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二级参考文献19

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  • 7Garcia- Cardena G, Fan R, Shah V, et al. Dynamic activation of endothelial nitric oxide synthase by Hsp90[J]. Nature, 1998,392(6678):821- 4.
  • 8Ou J, Fontana J T, Ou Z, et al. Heat shock protein 90 and tyrosine kinase regulate eNOS NO generation but not NO bioactivity[J]. Am J Physiol Heart Circ Physiol, 2004;286(2):H561- 9.
  • 9Ou J, Ou Z, Ackerman A W, et al. Inhibition of heat shock protein 90 (hsp90) in proliferating endothelial cells uncouples endothelial nitric oxide synthase activity[J]. Free Radic Biol Med, 2003, 34(2):269- 76.
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中山大学学报（医学科学版）
2004年 第6期

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