Cross-talk between SIRT1 and p66Shc in vascular diseases

被引:44
作者
Chen, Hou-Zao [1 ,2 ]
Wan, Yan-Zhen [1 ,2 ]
Liu, De-Pei [1 ,2 ]
机构
[1] Chinese Acad Med Sci, Inst Basic Med Sci, Dept Biochem & Mol Biol, State Key Lab Med Mol Biol, Beijing 100005, Peoples R China
[2] Peking Union Med Coll, Beijing 100005, Peoples R China
基金
中国国家自然科学基金;
关键词
OXIDATIVE STRESS; LIFE-SPAN; ADAPTER PROTEIN; ENDOTHELIAL DYSFUNCTION; LONGEVITY GENE; UP-REGULATION; CARDIOVASCULAR-DISEASE; PREMATURE SENESCENCE; MAMMALIAN SIRTUINS; DELETION;
D O I
10.1016/j.tcm.2013.01.001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Accumulating evidence indicates that oxidative stress can occur through overproduction of reactive oxygen species (ROS) and/or reduced anti-oxidant potentials under pathophysiological conditions and plays an important role in the development of cardiovascular diseases (CVDs). Adapter protein p66Shc has the property to directly stimulate mitochondrial ROS generation by an oxidoreductase activity. A growing body of evidence implies that p66Shc plays a critical role in the pathophysiology of age-related vascular diseases. Silent mating type information regulator 2 homolog 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent class III histone deacetylase (HDAC), has also been implicated in protection against vascular aging and age-related vascular diseases. Recently, we demonstrated that SIRT1 protects blood vessels from hyperglycemia-induced endothelial dysfunction through a novel mechanism involving the downregulation of p66Shc expression. In this review, we discuss the cross-talk between these two longevity genes as a mechanism of preventing vascular diseases by involving anti-oxidative stress responses and inhibiting endothelial senescence. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:237 / 241
页数:5
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