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REVIEW article

Front. Mol. Neurosci.
Sec. Molecular Signalling and Pathways
Volume 17 - 2024 | doi: 10.3389/fnmol.2024.1443401
This article is part of the Research Topic Pathobiological Defects in Sensorineural Hearing Loss: From Identification to Rescue View all 5 articles

Insights into the molecular underlying mechanisms and therapeutic potential of endoplasmic reticulum stress in sensorineural hearing loss

Provisionally accepted
Guanzhen Li Guanzhen Li 1Huiming Yang Huiming Yang 2Peiyuan Zhang Peiyuan Zhang 1*Yan Guo Yan Guo 3*Lili Yuan Lili Yuan 3*Shujiao Xu Shujiao Xu 4*Yingxue Yuan Yingxue Yuan 5*Huabao Xiong Huabao Xiong 6*Haiyan Yin Haiyan Yin 3*
  • 1 School of Clinical Medicine, Jining Medical University, Jining, China
  • 2 Department of Otolaryngology-Head and Neck Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China
  • 3 School of Basic Medical Science, Jining Key Laboratory of Pharmacology, Jining Medical University, Jining, China
  • 4 School of Dental Medicine, Jining Medical University, Jining, China
  • 5 Department of Pathology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China
  • 6 Institute of Immunology and Molecular Medicine, Jining Medical University, Jining, Shandong, China

The final, formatted version of the article will be published soon.

    Sensorineural hearing loss (SNHL) is characterized by a compromised cochlear perception of sound waves. Major risk factors for SNHL include genetic mutations, exposure to noise, ototoxic medications, and the aging process. Previous research has demonstrated that inflammation, oxidative stress, apoptosis, and autophagy, which are detrimental to inner ear cells, contribute to the pathogenesis of SNHL; however, the precise mechanisms remain inadequately understood. The endoplasmic reticulum (ER) plays a key role in various cellular processes, including protein synthesis, folding, lipid synthesis, cellular calcium and redox homeostasis, and its homeostatic balance is essential to maintain normal cellular function. Accumulation of unfolded or misfolded proteins in the ER leads to endoplasmic reticulum stress (ERS) and activates the unfolded protein response (UPR) signaling pathway. The adaptive UPR has the potential to reestablish protein homeostasis, whereas the maladaptive UPR, associated with inflammation, oxidative stress, apoptosis, and autophagy, can lead to cellular damage and death. Recent evidence increasingly supports the notion that ERS-mediated cellular damage responses play a crucial role in the initiation and progression of various SNHLs. This article reviews the research advancements on ERS in SNHL, with the aim of elucidating molecular biological mechanisms underlying ERS in SNHL and providing novel insights for the treatment.

    Keywords: sensorineural hearing loss, Endoplasmic Reticulum Stress, Unfolded Protein Response, Oxidative Stress, Apoptosis, Inflammation, Autophagy

    Received: 24 Jul 2024; Accepted: 03 Dec 2024.

    Copyright: © 2024 Li, Yang, Zhang, Guo, Yuan, Xu, Yuan, Xiong and Yin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Peiyuan Zhang, School of Clinical Medicine, Jining Medical University, Jining, China
    Yan Guo, School of Basic Medical Science, Jining Key Laboratory of Pharmacology, Jining Medical University, Jining, China
    Lili Yuan, School of Basic Medical Science, Jining Key Laboratory of Pharmacology, Jining Medical University, Jining, China
    Shujiao Xu, School of Dental Medicine, Jining Medical University, Jining, China
    Yingxue Yuan, Department of Pathology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China
    Huabao Xiong, Institute of Immunology and Molecular Medicine, Jining Medical University, Jining, Shandong, China
    Haiyan Yin, School of Basic Medical Science, Jining Key Laboratory of Pharmacology, Jining Medical University, Jining, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.