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

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

JOURNAL=Frontiers in Cell and Developmental Biology

VOLUME=11

YEAR=2023

URL=https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2023.1119773

DOI=10.3389/fcell.2023.1119773

ISSN=2296-634X

ABSTRACT=<p>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.</p>