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Licensed Unlicensed Requires Authentication Published by De Gruyter August 21, 2017

Insights in pathogenesis of multiple sclerosis: nitric oxide may induce mitochondrial dysfunction of oligodendrocytes

  • Minghong Lan , Xiaoyi Tang , Jie Zhang and Zhongxiang Yao ORCID logo EMAIL logo

Abstract

Demyelinating diseases, such as multiple sclerosis (MS), are kinds of common diseases in the central nervous system (CNS), and originated from myelin loss and axonal damage. Oligodendrocyte dysfunction is the direct reason of demyelinating lesions in the CNS. Nitric oxide (NO) plays an important role in the pathological process of demyelinating diseases. Although the neurotoxicity of NO is more likely mediated by peroxynitrite rather than NO itself, NO can impair oligodendrocyte energy metabolism through mediating the damaging of mitochondrial DNA, mitochondrial membrane and mitochondrial respiratory chain complexes. In the progression of MS, NO can mainly mediate demyelination, axonal degeneration and cell death. Hence, in this review, we extensively discuss endangerments of NO in oligodendrocytes (OLs), which is suggested to be the main mediator in demyelinating diseases, e.g. MS. We hypothesize that NO takes part in MS through impairing the function of monocarboxylate transporter 1, especially causing axonal degeneration. Then, it further provides a new insight that NO for OLs may be a reliable therapeutic target to ameliorate the course of demyelinating diseases.

Acknowledgments

This work was supported by grants from the National Natural Science Foundation of China (Grant no. 31371147).

  1. Conflict of interest statement: The authors have no conflict of interest to declare.

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Received: 2017-05-15
Accepted: 2017-06-15
Published Online: 2017-08-21
Published in Print: 2017-12-20

©2018 Walter de Gruyter GmbH, Berlin/Boston

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