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Licensed Unlicensed Requires Authentication Published by De Gruyter February 18, 2015

An evaluation of the links between microRNA, autophagy, and epilepsy

  • Jing Gan , Yi Qu , Jiao Li , Fengyan Zhao and Dezhi Mu EMAIL logo

Abstract

Epilepsy is a serious chronic neurologic disorder characterized by recurrent unprovoked seizures resulting from abnormal and highly synchronous neuronal discharges within the brain. Small noncoding RNAs, called microRNAs, play vital roles in epileptogenesis, with potential contributions as valuable biomarkers and targets for the treatment of epilepsy. To maintain cellular homeostasis, cellular components, such as organelles, proteins, protein complexes/oligomers, and pathogens, are delivered to the lysosome for degradation through a process called autophagy, which plays either a protective or a harmful role under epileptic stress. Several autophagic mechanisms have been implicated in epileptogenesis, including the mammalian target of rapamycin pathway, aberrant substrate accumulation, and the formation of epileptic networks. In addition, the regulation of autophagy through microRNAs (miRNAs) represents a novel posttranscriptional regulatory mechanism through ‘autophagamiRNAs’. The correlation between autophagy and miRNA has increased our understanding of the underlying pathogenesis of human diseases. Here, we review the current findings regarding the correlations between miRNA, autophagy, and epilepsy to provide a solid foundation for further examination of the miRNA-autophagy pathway involved in epilepsy pathophysiology.


Corresponding author: Dezhi Mu, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, China, e-mail: ; and Key Laboratory of Obstetric & Gynecologic and Pediatric Diseases and Birth Defects of Ministry of Education, Sichuan University, Chengdu 610041, China; and Department of Pediatrics, University of California, San Francisco, CA 94143, USA

Acknowledgments

This work was supported by the National Science Foundation of China (no. 81330016 and 31171020 to Dezhi Mu; no. 81172174 and 81270724 to Yi Qu), the Major State Basic Research Development Program (2013CB967404), the Grants from Ministry of Education of China (313037, 20110181130002, IRT0935), the Grant from State Commission of Science Technology of China (2012BAI04B04), the Grants from Science and Technology Bureau of Sichuan province (2011JTD0005), and the Grant of clinical discipline program (neonatology) from the Ministry of Health of China (1311200003303).

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Received: 2014-9-1
Accepted: 2014-11-5
Published Online: 2015-2-18
Published in Print: 2015-4-1

©2015 by De Gruyter

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