| Literature DB >> 33346118 |
Yeon Ju Kim1, Oak-Sung Choo2, Jin-Sol Lee3, Jeong Hun Jang1, Hyun Goo Woo4, Yun-Hoon Choung5.
Abstract
Clearance of dysfunctional mitochondria via mitophagy is essential for cell survival and cochlear functions. However, it is not clear which genes are significantly involved in this process. Here, we investigated the changes in mitophagy and mitophagy-associated genes in mouse auditory cells to determine a possible correlation between mitophagy and age-related hearing loss (ARHL). Here, we show that most transcripts associated with mitophagy were downregulated in an age-dependent manner. We identified one significant differentially expressed gene associated with mitophagy, BCL2 interacting protein 3-like (BNIP3L)/NIX. Mitophagy-inhibited cells with BNIP3L/NIX knockdown showed hyperresponsiveness to oxidative stress resulting in cell senescence with increased levels of TOMM20 and LC3B. Overexpression of BNIP3L/NIX promotes the degradation of TOMM20 and LC3B during premature cell senescence. In conclusion, BNIP3L/NIX may play an important role in mitochondria degradation maintaining cochlear cell homeostasis during the aging process of hearing.Entities:
Keywords: BNIP3L/NIX; age-related hearing loss; hair cell; mitophagy; spiral ganglion cell
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Year: 2020 PMID: 33346118 DOI: 10.1016/j.neuroscience.2020.12.005
Source DB: PubMed Journal: Neuroscience ISSN: 0306-4522 Impact factor: 3.590