Mitochondrial dysfunction in hearing loss: Oxidative stress, autophagy and NLRP3 inflammasome

Peipei Li; Peipei Li; Shen Li; Le Wang; Hongmin Li; Yang Wang; Hongbing Liu; Xin Wang; Xiaodan Zhu; Zhangsuo Liu; Zhangsuo Liu; Fanglei Ye; Yuan Zhang

doi:10.3389/fcell.2023.1119773

Frontiers in Cell and Developmental Biology (Feb 2023)

Mitochondrial dysfunction in hearing loss: Oxidative stress, autophagy and NLRP3 inflammasome

Peipei Li,
Peipei Li,
Shen Li,
Le Wang,
Hongmin Li,
Yang Wang,
Hongbing Liu,
Xin Wang,
Xiaodan Zhu,
Zhangsuo Liu,
Zhangsuo Liu,
Fanglei Ye,
Yuan Zhang

Affiliations

Peipei Li: Department of Integrated Traditional and Western Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Peipei Li: Henan Province Research Center for Kidney Disease, Zhengzhou, China
Shen Li: Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Le Wang: Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Hongmin Li: Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Yang Wang: Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Hongbing Liu: Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Xin Wang: Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Xiaodan Zhu: Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Zhangsuo Liu: Department of Integrated Traditional and Western Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Zhangsuo Liu: Henan Province Research Center for Kidney Disease, Zhengzhou, China
Fanglei Ye: Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Yuan Zhang: Department of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China

DOI: https://doi.org/10.3389/fcell.2023.1119773
Journal volume & issue: Vol. 11

Abstract

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Sensorineural deafness becomes an inevitable worldwide healthy problem, yet the current curative therapy is limited. Emerging evidences demonstrate mitochondrial dysfunction plays a vital role of in the pathogenesis of deafness. Reactive oxygen species (ROS)-induced mitochondrial dysfunction combined with NLRP3 inflammasome activation is involved in cochlear damage. Autophagy not only clears up undesired proteins and damaged mitochondria (mitophagy), but also eliminate excessive ROS. Appropriate enhancement of autophagy can reduce oxidative stress, inhibit cell apoptosis, and protect auditory cells. In addition, we further discuss the interplays linking ROS generation, NLRP3 inflammasome activation, and autophagy underlying the pathogenesis of deafness, including ototoxic drugs-, noise- and aging-related hearing loss.

Published in Frontiers in Cell and Developmental Biology

ISSN: 2296-634X (Online)
Publisher: Frontiers Media S.A.
Country of publisher: Switzerland
LCC subjects: Science: Biology (General)
Website: https://www.frontiersin.org/journals/cell-and-developmental-biology

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