Canonical MAPK signaling in auditory neuropathy

Yueying Wang; Lusha Huang; Xiaoqing Cen; Yue Liang; Kaitian Chen

doi:10.1016/j.bbadis.2024.167619

Canonical MAPK signaling in auditory neuropathy

Biochim Biophys Acta Mol Basis Dis. 2024 Dec 9;1871(3):167619. doi: 10.1016/j.bbadis.2024.167619. Online ahead of print.

Authors

Yueying Wang¹, Lusha Huang¹, Xiaoqing Cen¹, Yue Liang¹, Kaitian Chen²

Affiliations

¹ Otorhinolaryngology Hospital, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China; Institute of Otorhinolaryngology, Sun Yat-sen University, Guangzhou 510080, China.
² Otorhinolaryngology Hospital, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China; Institute of Otorhinolaryngology, Sun Yat-sen University, Guangzhou 510080, China. Electronic address: chenkd6@mail.sysu.edu.cn.

PMID: 39662753
DOI: 10.1016/j.bbadis.2024.167619

Abstract

Auditory neuropathy (AN) is an under-recognized form of hearing loss characterized by lesions in inner hair cells (IHCs), ribbon synapses and spiral ganglion neurons (SGNs). The lack of a targeted therapy for AN has increased the need for a better understanding of the pathogenic mechanism of AN. As mitogen-activated protein kinase (MAPK) signaling is ubiquitous in many biological processes, its alteration may facilitate the pathogenesis of multiple sites in AN. Here, we summaries the characteristics of AN under different molecular bases and first explore the mechanism of MAPK at different lesion sites. Alterations of extracellular signal-regulated kinase (ERK)/MAPK occur in IHCs and SGNs, whereas modulations of p38 and c-Jun NH2-terminal kinase (JNK) were found in ribbon synapses and SGNs. In conclusion, inductive MAPK alterations in the pathogenesis and development of AN are likely to represent a potential therapeutic target to guide the development of treatments.

Keywords: Auditory neuropathy; Hearing loss; MAPK; Mitogen-activated protein kinase; Pathogenesis.

Publication types

Review