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本文引用的文献

1
Cellular metabolic stress: considering how cells respond to nutrient excess.细胞代谢应激:探讨细胞如何应对营养过剩。
Mol Cell. 2010 Oct 22;40(2):323-32. doi: 10.1016/j.molcel.2010.10.004.
2
Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress.营养物质、生长因子和应激对 mTOR 复合物 1 通路的调节。
Mol Cell. 2010 Oct 22;40(2):310-22. doi: 10.1016/j.molcel.2010.09.026.
3
miR-210 is overexpressed in late stages of lung cancer and mediates mitochondrial alterations associated with modulation of HIF-1 activity.miR-210 在肺癌晚期过表达,并介导与 HIF-1 活性调节相关的线粒体改变。
Cell Death Differ. 2011 Mar;18(3):465-78. doi: 10.1038/cdd.2010.119. Epub 2010 Oct 1.
4
Chronic inhibition of hypoxia-inducible factor prolyl 4-hydroxylase improves ventricular performance, remodeling, and vascularity after myocardial infarction in the rat.慢性抑制缺氧诱导因子脯氨酰 4-羟化酶可改善大鼠心肌梗死后心室功能、重构和血管生成。
J Cardiovasc Pharmacol. 2010 Aug;56(2):147-55. doi: 10.1097/FJC.0b013e3181e2bfef.
5
Metabolic analysis of 13C-labeled pyruvate for noninvasive assessment of mitochondrial function.13C 标记丙酮酸的代谢分析用于无创评估线粒体功能。
Ann N Y Acad Sci. 2010 Jul;1201:111-20. doi: 10.1111/j.1749-6632.2010.05636.x.
6
Hypoxia-regulated microRNA-210 modulates mitochondrial function and decreases ISCU and COX10 expression.缺氧调节 microRNA-210 调节线粒体功能并降低 ISCU 和 COX10 的表达。
Oncogene. 2010 Jul 29;29(30):4362-8. doi: 10.1038/onc.2010.193. Epub 2010 May 24.
7
MicroRNA-210 regulates mitochondrial free radical response to hypoxia and krebs cycle in cancer cells by targeting iron sulfur cluster protein ISCU.MicroRNA-210 通过靶向铁硫簇蛋白 ISCU 调节癌细胞对缺氧和克雷布斯循环的线粒体自由基反应。
PLoS One. 2010 Apr 26;5(4):e10345. doi: 10.1371/journal.pone.0010345.
8
Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes.线粒体活性氧调节细胞信号转导并决定生物学结果。
Trends Biochem Sci. 2010 Sep;35(9):505-13. doi: 10.1016/j.tibs.2010.04.002. Epub 2010 Apr 27.
9
Human brown adipose tissue.人体棕色脂肪组织。
Cell Metab. 2010 Apr 7;11(4):248-52. doi: 10.1016/j.cmet.2010.03.008.
10
Hearts of hypoxia-inducible factor prolyl 4-hydroxylase-2 hypomorphic mice show protection against acute ischemia-reperfusion injury.低氧诱导因子脯氨酰 4-羟化酶-2 功能减弱型小鼠的心脏对急性缺血再灌注损伤具有保护作用。
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缺氧。2. 缺氧调节细胞代谢。

Hypoxia. 2. Hypoxia regulates cellular metabolism.

机构信息

Division of Pulmonary & Critical Care Medicine, 240 East Huron Ave., McGraw M-334, Chicago, IL 60611-2909, USA.

出版信息

Am J Physiol Cell Physiol. 2011 Mar;300(3):C385-93. doi: 10.1152/ajpcell.00485.2010. Epub 2010 Dec 1.

DOI:10.1152/ajpcell.00485.2010
PMID:21123733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3063979/
Abstract

Adaptation to lowering oxygen levels (hypoxia) requires coordinated downregulation of metabolic demand and supply to prevent a mismatch in ATP utilization and production that might culminate in a bioenergetic collapse. Hypoxia diminishes ATP utilization by downregulating protein translation and the activity of the Na-K-ATPase. Hypoxia diminishes ATP production in part by lowering the activity of the electron transport chain through activation of the transcription factor hypoxia-inducible factor-1. The decrease in electron transport limits the overproduction of reactove oxygen species during hypoxia and slows the rate of oxygen depletion to prevent anoxia. In this review, we discuss these mechanisms that diminish metabolic supply and demand for adaptation to hypoxia.

摘要

适应低氧水平(缺氧)需要协调下调代谢需求和供应,以防止 ATP 利用和产生之间的不匹配,否则可能导致生物能量崩溃。缺氧通过下调蛋白质翻译和 Na-K-ATP 酶的活性来减少 ATP 的利用。缺氧部分通过激活转录因子缺氧诱导因子-1 来降低电子传递链的活性来减少 ATP 的产生。电子传递的减少限制了缺氧期间活性氧物质的过度产生,并减缓了氧气消耗的速度,以防止缺氧。在这篇综述中,我们讨论了这些机制,这些机制可以减少代谢供应和需求,以适应缺氧。