Autophagy Regulates the Survival of Hair Cells and Spiral Ganglion Neurons in Cases of Noise, Ototoxic Drug, and Age-Induced Sensorineural Hearing Loss.

Lingna Guo,Jianming Yang,Shuangba He,Wei Cao,Yuguang Niu,Renjie Chai

doi:10.3389/fncel.2021.760422

Abstract

Inner ear hair cells (HCs) and spiral ganglion neurons (SGNs) are the core components of the auditory system. However, they are vulnerable to genetic defects, noise exposure, ototoxic drugs and aging, and loss or damage of HCs and SGNs results in permanent hearing loss due to their limited capacity for spontaneous regeneration in mammals. Many efforts have been made to combat hearing loss including cochlear implants, HC regeneration, gene therapy, and antioxidant drugs. Here we review the role of autophagy in sensorineural hearing loss and the potential targets related to autophagy for the treatment of hearing loss.

Highlights

According to the World Health Organization (WHO, 2021), about 5% of the world’s population suffer from hearing impairment, and it is expected that the number of people with disabling hearing loss will be around 700 million by 2050
We present the role of autophagy in hearing loss induced by noise exposure, ototoxic drugs and aging, and describe the molecules and signaling pathways involved in autophagy in the inner ear
Excessive autophagy can lead to cell death under some conditions, activation of autophagy protects hair cells (HCs) and spiral ganglion neurons (SGNs) against oxidative stress-induced death

Summary

Introduction

According to the World Health Organization (WHO, 2021), about 5% of the world’s population (or 430 million people) suffer from hearing impairment, and it is expected that the number of people with disabling hearing loss will be around 700 million by 2050. Autophagy has been reported to play an antioxidative role in preventing sensorineural hearing loss (SNHL) (Ye et al, 2019a). We present the role of autophagy in hearing loss induced by noise exposure, ototoxic drugs and aging, and describe the molecules and signaling pathways involved in autophagy in the inner ear.

Results

Conclusion