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本文引用的文献

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Proapoptotic BAX and BAK regulate the type 1 inositol trisphosphate receptor and calcium leak from the endoplasmic reticulum.促凋亡蛋白BAX和BAK调节1型肌醇三磷酸受体以及内质网的钙泄漏。
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Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair.胸腺素β4激活整合素连接激酶并促进心脏细胞迁移、存活及心脏修复。
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The mitochondrial death pathway and cardiac myocyte apoptosis.线粒体死亡途径与心肌细胞凋亡
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Translocation of Bim to the endoplasmic reticulum (ER) mediates ER stress signaling for activation of caspase-12 during ER stress-induced apoptosis.Bim转位至内质网介导内质网应激信号,在内质网应激诱导的细胞凋亡过程中激活半胱天冬酶-12。
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Prolonged endoplasmic reticulum stress in hypertrophic and failing heart after aortic constriction: possible contribution of endoplasmic reticulum stress to cardiac myocyte apoptosis.主动脉缩窄后肥厚及衰竭心脏中的内质网应激延长:内质网应激对心肌细胞凋亡的可能作用
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死亡导致心脏功能衰竭。

Death begets failure in the heart.

作者信息

Foo Roger S-Y, Mani Kartik, Kitsis Richard N

机构信息

Department of Medicine, Cardiovascular Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

出版信息

J Clin Invest. 2005 Mar;115(3):565-71. doi: 10.1172/JCI24569.

DOI:10.1172/JCI24569
PMID:15765138
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1052022/
Abstract

Recently, low--but abnormal--rates of cardiomyocyte apoptosis have been observed in failing human hearts. Genetic and pharmacological studies suggest that this cell death is causally linked to heart failure in rodent models. Herein, we review these data and discuss potential therapeutic implications.

摘要

最近,在衰竭的人类心脏中观察到心肌细胞凋亡率较低但异常。遗传学和药理学研究表明,在啮齿动物模型中,这种细胞死亡与心力衰竭存在因果关系。在此,我们回顾这些数据并讨论潜在的治疗意义。