Overcoming an energy crisis?: an adaptive role of glycogen synthase kinase-3 inhibition in ischemia/reperfusion.
作者信息
Zhai Peiyong, Sadoshima Junichi
出版信息
Circ Res. 2008 Oct 24;103(9):910-3. doi: 10.1161/01.RES.0000338259.37472.b6.
Abstract
摘要
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Overcoming an energy crisis?: an adaptive role of glycogen synthase kinase-3 inhibition in ischemia/reperfusion.克服能量危机？糖原合酶激酶-3抑制在缺血/再灌注中的适应性作用
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本文引用的文献
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Glycogen synthase kinase 3 inhibition slows mitochondrial adenine nucleotide transport and regulates voltage-dependent anion channel phosphorylation.糖原合酶激酶3抑制作用减缓线粒体腺嘌呤核苷酸转运并调节电压依赖性阴离子通道磷酸化。
Circ Res. 2008 Oct 24;103(9):983-91. doi: 10.1161/CIRCRESAHA.108.178970. Epub 2008 Sep 18.
2
Exogenous zinc protects cardiac cells from reperfusion injury by targeting mitochondrial permeability transition pore through inactivation of glycogen synthase kinase-3beta.外源性锌通过使糖原合酶激酶-3β失活来靶向线粒体通透性转换孔，从而保护心脏细胞免受再灌注损伤。
Am J Physiol Heart Circ Physiol. 2008 Sep;295(3):H1227-H1233. doi: 10.1152/ajpheart.00610.2008. Epub 2008 Jul 25.
3
Glycogen synthase kinase-3 inactivation is not required for ischemic preconditioning or postconditioning in the mouse.糖原合酶激酶-3失活对小鼠缺血预处理或后处理并非必需。
Circ Res. 2008 Aug 1;103(3):307-14. doi: 10.1161/CIRCRESAHA.107.169953. Epub 2008 Jun 26.
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Inhibition of GSK3beta by postconditioning is required to prevent opening of the mitochondrial permeability transition pore during reperfusion.后适应对GSK3β的抑制作用是防止再灌注期间线粒体通透性转换孔开放所必需的。
Circulation. 2008 May 27;117(21):2761-8. doi: 10.1161/CIRCULATIONAHA.107.755066. Epub 2008 May 19.
5
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Modulation of the mitochondrial permeability transition pore complex in GSK-3beta-mediated myocardial protection.糖原合成酶激酶-3β介导的心肌保护中线粒体通透性转换孔复合物的调节
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Glycogen synthase kinase 3alpha-specific regulation of murine hepatic glycogen metabolism.糖原合酶激酶3α对小鼠肝脏糖原代谢的特异性调控
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