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腺苷酸活化蛋白激酶在脂联素心血管保护效应中的作用

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李丽 吴立玲

北京大学医学部生理与病理生理学系,教育部分子心血管重点实验室,北京100083

生理学报
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国际标准刊号:ISSN 0371-0874
国内统一刊号:CN 31-1352

摘  要:

脂联素是主要由白色脂肪组织分泌的一种活性多肽,具有调节脂肪酸和葡萄糖代谢、抗炎、减轻动脉粥样硬化等多种生物学功能,血浆脂联素含量降低参与了代谢性疾病及心血管疾病的发生、发展。腺苷酸活化蛋白激酶(AMP.activated protein kinase,AMPK)是脂联素信号通路中的关键信号分子,本文就其在脂联素心血管保护效应中的作用作一综述,介绍脂联素改善糖、脂代谢紊乱、动脉粥样硬化、心力衰竭及心肌缺血,再灌注损伤作用机制的新进展。[著者文摘]

文章出处:

《生理学报》-2007年59卷5期 -614-618页

Acta Physiologica Sinica

栏目信息:

综述

分 类 号:

R363

相关文章:

参考文献(29篇) 耦合文献(2篇)  主题相关

[参考文献]

Effect of AMP-activated protein kinase on cardiovascular protection of adiponectin

I Li, WU Li-Ling Department of Physiology and Pathophysiology, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University Health Science Center, Beifing 100083, China

Abstract:

Adiponectin, derived mainly from white adipose tissue, regulates glucose and fatty acid metabolism and has anti-inflamma- tory and anti-atherosclerotic properties. The decrease in plasma adiponectin concentration contributes to the development of metabolic and cardiovascular diseases. AMP-activated protein kinase (AMPK) is a serine/threonine kinase which plays an important role in regulating many cellular processes, particularly pathways involved in cellular energy status. AMPK is now recognized as a fuel gauge in mammalian cells. Adiponectin activates AMPK phosphorylation and then promotes ATP-generating pathways in heart, including glucose transport, glycolysis, and fatty acid oxidation. The recent evidence has shown that AMPK activation has an important role in the vasculature where it may exert anti-atherosclerotic effects. Phosphorylation of AMPK induced by adiponectin inhibits protein synthesis, and may be an adaptive response to pathological cardiac hypertrophy. AMPK also has a cardioprotective role against myocardial injury and apoptosis in the ischemic heart. This review will discuss the role of AMPK in adiponectin-mediated protective properties of cardiovascular diseases.[著者文摘]

Key words:

adiponectin; AMP-activated protein kinase; cardiovascular protection

收稿日期: 2007-07-09
修订日期: 2007-08-23

基金资助:

This work was supported by the National Natural Science Foundation of China (No. 30570715) and the Program tor Changllang Scholars and Innovative Research Team in University of China.

作者简介:

Correspondingauthor.Tel:+86-10-82802403;Fax:+86-10-82802403;E-mail:pathophy@bjmu.edu.cn

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