Suppr超能文献

线粒体代谢:神经炎症与神经退行性变之间的共同联系。

Mitochondrial metabolism: a common link between neuroinflammation and neurodegeneration.

作者信息

Garabadu Debapriya, Agrawal Nidhi, Sharma Anjali, Sharma Sahil

机构信息

Division of Pharmacology, Institute of Pharmaceutical Research, GLA University, Mathura, India.

出版信息

Behav Pharmacol. 2019 Dec;30(8):642-652. doi: 10.1097/FBP.0000000000000505.

Abstract

Neurodegenerative disorders have been considered as a growing health concern for decades. Increasing risk of neurodegenerative disorders creates a socioeconomic burden to both patients and care givers. Mitochondria are organelle that are involved in both neuroinflammation and neurodegeneration. There are few reports on the effect of mitochondrial metabolism on the progress of neurodegeneration and neuroinflammation. Therefore, the present review summarizes the potential contribution of mitochondrial metabolic pathways in the pathogenesis of neuroinflammation and neurodegeneration. Mitochondrial pyruvate metabolism plays a critical role in the pathogenesis of neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. However, there its potential contribution in other neurodegenerative disorders is as yet unproven. The mitochondrial pyruvate carrier and pyruvate dehydrogenase can modulate mitochondrial pyruvate metabolism to attenuate neuroinflammation and neurodegeneration. Further, it has been observed that the mitochondrial citric acid cycle can regulate the pathogenesis of neuroinflammation and neurodegeneration. Additional research should be undertaken to target tricarboxylic acid cycle enzymes to minimize the progress of neuroinflammation and neurodegeneration. It has also been observed that the mitochondrial urea cycle can potentially contribute to the progression of neurodegenerative disorders. Therefore, targeting this pathway may control the mitochondrial dysfunction-induced neuroinflammation and neurodegeneration. Furthermore, the mitochondrial malate-aspartate shuttle could be another target to control mitochondrial dysfunction-induced neuroinflammation and neurodegeneration in neurodegenerative disorders.

摘要

几十年来,神经退行性疾病一直被视为日益严重的健康问题。神经退行性疾病风险的增加给患者和护理人员都带来了社会经济负担。线粒体是参与神经炎症和神经退行性变的细胞器。关于线粒体代谢对神经退行性变和神经炎症进展的影响,报道较少。因此,本综述总结了线粒体代谢途径在神经炎症和神经退行性病变发病机制中的潜在作用。线粒体丙酮酸代谢在帕金森病和阿尔茨海默病等神经退行性疾病的发病机制中起关键作用。然而,其在其他神经退行性疾病中的潜在作用尚未得到证实。线粒体丙酮酸载体和丙酮酸脱氢酶可以调节线粒体丙酮酸代谢,以减轻神经炎症和神经退行性变。此外,据观察,线粒体柠檬酸循环可以调节神经炎症和神经退行性变的发病机制。应该针对三羧酸循环酶进行更多研究,以尽量减少神经炎症和神经退行性变的进展。还观察到线粒体尿素循环可能促进神经退行性疾病的进展。因此,针对这一途径可能控制线粒体功能障碍引起的神经炎症和神经退行性变。此外,线粒体苹果酸 - 天冬氨酸穿梭可能是控制神经退行性疾病中线粒体功能障碍引起的神经炎症和神经退行性变的另一个靶点。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验