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首页> 外文期刊>Translational Stroke Research >Mitochondrial Dysfunction and NAD+ Metabolism Alterations in the Pathophysiology of Acute Brain Injury
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Mitochondrial Dysfunction and NAD+ Metabolism Alterations in the Pathophysiology of Acute Brain Injury

机译：急性脑损伤的病理生理学中的线粒体功能障碍和NAD +代谢改变。

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摘要

Mitochondrial dysfunction is commonly believed to be one of the major players in mechanisms of brain injury. For several decades, pathologic mitochondrial calcium overload and associated opening of the mitochondrial permeability transition (MPT) pore were considered a detrimental factor causing mitochondrial damage and bioenergetics failure. Mitochondrial and cellular bioenergetic metabolism depends on the enzymatic reactions that require NAD+ or its reduced form NADH as cofactors. Recently, it was shown that NAD+ also has an important function as a substrate for several NAD+ glycohydrolases whose overactivation can contribute to cell death mechanisms. Furthermore, downstream metabolites of NAD+ catabolism can also adversely affect cell viability. In contrast to the negative effects of NAD+-catabolizing enzymes, enzymes that constitute the NAD+ biosynthesis pathway possess neuroprotective properties. In the first part of this review, we discuss the role of MPT in acute brain injury and its role in mitochondrial NAD+ metabolism. Next, we focus on individual NAD+ glycohydrolases, both cytosolic and mitochondrial, and their role in NAD+ catabolism and brain damage. Finally, we discuss the potential effects of downstream products of NAD+ degradation and associated enzymes as well as the role of NAD+ resynthesis enzymes as potential therapeutic targets.
机译：通常认为线粒体功能障碍是脑损伤机制的主要参与者之一。几十年来，病理性线粒体钙超载和相关的线粒体通透性转变（MPT）孔的开放被认为是导致线粒体损伤和生物能学失败的有害因素。线粒体和细胞的生物能代谢取决于需要NAD +或其还原形式的NADH作为辅因子的酶促反应。最近，已显示出NAD +还具有作为几种NAD +糖水解酶的底物的重要功能，它们的过度活化可能有助于细胞死亡机制。此外，NAD +分解代谢的下游代谢产物也可能对细胞活力产生不利影响。与NAD +分解酶的负面影响相反，构成NAD +生物合成途径的酶具有神经保护特性。在这篇综述的第一部分中，我们讨论了MPT在急性脑损伤中的作用及其在线粒体NAD +代谢中的作用。接下来，我们重点研究细胞溶质和线粒体的单个NAD +糖水解酶及其在NAD +分解代谢和脑损伤中的作用。最后，我们讨论了NAD +降解下游产物和相关酶的潜在作用，以及NAD +再合成酶作为潜在治疗靶标的作用。

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  • 来源
    《Translational Stroke Research》 |2013年第6期|618-634|共17页
  • 作者

    Katrina Owens; Ji H. Park; Rosemary Schuh; Tibor Kristian;

  • 作者单位

    Veterans Affairs Maryland Health Care System">(1);

    Veterans Affairs Maryland Health Care System">(1);

    Veterans Affairs Maryland Health Care System">(1);

    Department of Neurology School of Medicine University of Maryland Baltimore">(3);

    Veterans Affairs Maryland Health Care System">(1);

    Department of Anesthesiology Center for Shock Trauma and Anesthesiology Research School of Medicine University of Maryland Baltimore">(2);

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  • 正文语种 eng
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  • 关键词

    Mitochondria; Nicotinamide adenine dinucleotide; Ischemia; Brain;

    机译：线粒体;烟酰胺腺嘌呤二核苷酸;缺血;脑;

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