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心肌缺血——代谢途径及糖酵解增加的影响

Myocardial ischemia--metabolic pathways and implications of increased glycolysis.

作者信息

Opie L H

机构信息

Medical Research Council, University of Cape Town Ischaemic Heart Disease Research Unit, South Africa.

出版信息

Cardiovasc Drugs Ther. 1990 Aug;4 Suppl 4:777-90. doi: 10.1007/BF00051275.

DOI:10.1007/BF00051275
PMID:1965525
Abstract

Evidence is reviewed that favors the hypothesis that maintenance of glycolysis plays a special role in protecting membrane function in ischemia. Therefore all procedures stimulating glycolytic flux should be beneficial in ischemia, and procedures inhibiting flux should be harmful. However, a crucial consideration is the coronary flow rate. In severe ischemia, accumulation of protons, derived not directly from glycolytic flux but from the breakdown of ATP and from proton-producing cycles, will tend to inhibit glycolysis and to minimize any benefit from increased glycolytic flux. Therefore maintenance of intracellular pH is crucial to the concept of the benefits of glycolysis. It also follows that the severity of ischemia can determine whether or not enhanced glycolysis has a beneficial effect. It is argued that a multiple approach, including enhanced glycolytic flux, control of intracellular pH, and improved coronary flow, constitutes the combination most likely to benefit ischemia.

摘要

有证据支持这样一种假说

糖酵解的维持在缺血时保护膜功能方面发挥特殊作用。因此,所有刺激糖酵解通量的程序在缺血时应是有益的,而抑制通量的程序则应是有害的。然而,一个关键的考虑因素是冠状动脉血流速度。在严重缺血时,质子的积累并非直接源于糖酵解通量,而是来自ATP的分解和产质子循环,这将倾向于抑制糖酵解,并使糖酵解通量增加带来的任何益处最小化。因此,维持细胞内pH对于糖酵解有益这一概念至关重要。由此还可推断,缺血的严重程度可决定增强的糖酵解是否具有有益效果。有人认为,包括增强糖酵解通量、控制细胞内pH和改善冠状动脉血流在内的多种方法构成了最有可能使缺血受益的组合。

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本文引用的文献

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The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus.葡萄糖脂肪酸循环。其在胰岛素敏感性及糖尿病代谢紊乱中的作用。
Lancet. 1963 Apr 13;1(7285):785-9. doi: 10.1016/s0140-6736(63)91500-9.
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The time of onset and severity of acidosis in myocardial ischaemia.心肌缺血时酸中毒的发作时间和严重程度。
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The influence of ATP depletion on the action of phospholipase C on cardiac myocyte membrane phospholipids.
去泛素化酶 OTUD4 通过上调糖酵解酶 PFKFB3 促进心肌梗死后的心脏纤维化。
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Metabolic Regulation of Cardiac Regeneration.心脏再生的代谢调控
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Curr Heart Fail Rep. 2022 Aug;19(4):180-190. doi: 10.1007/s11897-022-00554-1. Epub 2022 May 14.
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Roles of MicroRNAs in Glucose and Lipid Metabolism in the Heart.微小RNA在心脏葡萄糖和脂质代谢中的作用
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