Mitochondrial redox system: A key target of antioxidant therapy to prevent acquired sensorineural hearing loss

Jeong-In Baek; Ye-Ri Kim; Kyu-Yup Lee; Un-Kyung Kim

doi:10.3389/fphar.2023.1176881

Mitochondrial redox system: A key target of antioxidant therapy to prevent acquired sensorineural hearing loss

Front Pharmacol. 2023 Mar 31:14:1176881. doi: 10.3389/fphar.2023.1176881. eCollection 2023.

Authors

Jeong-In Baek¹, Ye-Ri Kim^{2

3}, Kyu-Yup Lee⁴, Un-Kyung Kim^{2

5}

Affiliations

¹ Department of Companion Animal Health, College of Rehabilitation and Health, Daegu Haany University, Gyeongsan, Republic of Korea.
² Department of Biology, College of Natural Sciences, Kyungpook National University, Daegu, Republic of Korea.
³ Advanced Bio-Resource Research Center, Kyungpook National University, Daegu, Republic of Korea.
⁴ Department of Otorhinolaryngology-Head and Neck Surgery, School of Medicine, Kyungpook National University, Daegu, Republic of Korea.
⁵ School of Life Sciences, KNU Creative BioResearch Group (BK21 Plus Project), Kyungpook National University, Daegu, Republic of Korea.

Abstract

Noise (noise-induced hearing loss), and ototoxic drugs (drug-induced ototoxicity), and aging (age-related hearing loss) are the major environmental factors that lead to acquired sensorineural hearing loss. So far, there have been numerous efforts to develop protective or therapeutic agents for acquired hearing loss by investigating the pathological mechanisms of each types of hearing loss, especially in cochlear hair cells and auditory nerves. Although there is still a lack of information on the underlying mechanisms of redox homeostasis and molecular redox networks in hair cells, an imbalance in mitochondrial reactive oxygen species (ROS) levels that enhance oxidative stress has been suggested as a key pathological factor eventually causing acquired sensorineural hearing loss. Thus, various types of antioxidants have been investigated for their abilities to support auditory cells in maintenance of the hearing function against ototoxic stimuli. In this review, we will discuss the scientific possibility of developing drugs that target particular key elements of the mitochondrial redox network in prevention or treatment of noise- and ototoxic drug-induced hearing loss.

Keywords: ROS; acquired hearing loss; drug development; mitochondria; noise; ototoxic drugs.

Publication types

Review

Grants and funding

This research was supported by the National Research Foundation of Korea (NRF) Grant funded by the Korea government (Ministry of Science and ICT): RS-2023-00212674 (to J-IB), NRF-2020R1A2C2003529 (to K-YL), and NRF-2021R1C1C2006677 (to Y-RK). It was also supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MSIT), No. 2022M3E5F2017487 (to U-KK).