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单羧酸转运蛋白1可能有益于脑缺血,促进乳酸从神经胶质细胞向神经元的转运。

Monocarboxylate Transporter 1 May Benefit Cerebral Ischemia Facilitating Lactate Transport From Glial Cells to Neurons.

作者信息

Zhang Mao, Wang Yanyan, Bai Yun, Dai Limeng, Guo Hong

机构信息

Department of Medical Genetics, College of Basic Medical Sciences, Army Medical University, Chongqing, China.

出版信息

Front Neurol. 2022 Apr 25;13:781063. doi: 10.3389/fneur.2022.781063. eCollection 2022.

DOI:10.3389/fneur.2022.781063
PMID:35547368
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9081727/
Abstract

Monocarboxylate transporter 1 (MCT1) is expressed in glial cells and some populations of neurons. MCT1 facilitates astrocytes or oligodendrocytes (OLs) in the energy supplement of neurons, which is crucial for maintaining the neuronal activity and axonal function. It is suggested that MCT1 upregulation in cerebral ischemia is protective to ischemia/reperfusion (I/R) injury. Otherwise, its underlying mechanism has not been clearly discussed. In this review, it provides a novel insight that MCT1 may protect brain from I/R injury facilitating lactate transport from glial cells (such as, astrocytes and OLs) to neurons. It extensively discusses (1) the structure and localization of MCT1; (2) the regulation of MCT1 in lactate transport among astrocytes, OLs, and neurons; and (3) the regulation of MCT1 in the cellular response of lactate accumulation under ischemic attack. At last, this review concludes that MCT1, in cerebral ischemia, may improve lactate transport from glial cells to neurons, which subsequently alleviates cellular damage induced by lactate accumulation (mostly in glial cells), and meets the energy metabolism of neurons.

摘要

单羧酸转运蛋白1(MCT1)在神经胶质细胞和一些神经元群体中表达。MCT1促进星形胶质细胞或少突胶质细胞(OLs)为神经元补充能量,这对维持神经元活动和轴突功能至关重要。有研究表明,脑缺血时MCT1上调对缺血/再灌注(I/R)损伤具有保护作用。然而,其潜在机制尚未得到明确探讨。在本综述中,提出了一个新的观点,即MCT1可能通过促进乳酸从神经胶质细胞(如星形胶质细胞和OLs)向神经元的转运来保护大脑免受I/R损伤。本文广泛讨论了:(1)MCT1的结构和定位;(2)MCT1在星形胶质细胞、OLs和神经元之间乳酸转运中的调节作用;(3)缺血攻击下MCT1在乳酸积累的细胞反应中的调节作用。最后,本综述得出结论,在脑缺血中,MCT1可能改善乳酸从神经胶质细胞向神经元的转运,从而减轻乳酸积累(主要在神经胶质细胞中)引起的细胞损伤,并满足神经元的能量代谢需求。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbbe/9081727/030c94c6d392/fneur-13-781063-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbbe/9081727/2c89c20d4de9/fneur-13-781063-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbbe/9081727/ec3b9a19a365/fneur-13-781063-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbbe/9081727/030c94c6d392/fneur-13-781063-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbbe/9081727/2c89c20d4de9/fneur-13-781063-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbbe/9081727/ec3b9a19a365/fneur-13-781063-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbbe/9081727/030c94c6d392/fneur-13-781063-g0003.jpg

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