ArticleMolecular brain2021
Cdk5 regulatory subunit-associated protein 1 knockout mice show hearing loss phenotypically similar to age-related hearing loss.
Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- A Systematic Review of Genes Affecting Endocochlear Potential.Journal of the Association for Research in Otolaryngology : JARO · 2026Pooled it
- Therapeutic Timing at Mitochondrial Redox-Autophagy-Mitophagy Checkpoints in Age-Related Hearing Loss.Molecular neurobiology · 2026Review
- Blood-labyrinth barrier disruption associates with hypercholesterolemia-induced hearing loss.iScience · 2026Article
- The Role and Research Progress of Mitochondria in Sensorineural Hearing Loss.Molecular neurobiology · 2025Review
- Article
- Article
- Mitochonic acid 5 mitigates age-related hearing loss progression by targeting defective 2-methylthiolation in mitochondrial transfer RNAs.Frontiers in cellular neuroscience · 2025Article
- Histopathological change of age-related hearing loss in female advance-aged CBA/CaJ mice.PloS one · 2025Article
- Research Advances on Deafness Genes Associated with Mitochondrial tRNA-37 Modifications.The journal of international advanced otology · 2023Review
- Mitochondrial alterations in the cochlea of Cdk5rap1-knockout mice with age-related hearing loss.FEBS open bio · 2023Article
- Aging and aging-related diseases: from molecular mechanisms to interventions and treatments.Signal transduction and targeted therapy · 2022Review
- Modifications of the human tRNA anticodon loop and their associations with genetic diseases.Cellular and molecular life sciences : CMLS · 2021Review
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is associated with aging and age-related hearing loss (AHL). However, the precise mechanisms underlying the pathophysiology of hearing loss remain unclear. Cdk5 regulatory subunit-associated protein 1 (CDK5RAP1) enables efficient intramitochondrial translation by catalyzing the deposition of 2-methylthio modifications on mitochondrial tRNAs. Here we investigated the effect of defective mitochondrial protein translation on hearing and AHL in a Cdk5rap1 deficiency C57BL/6 mouse model. Compared to control C57BL/6 mice, Cdk5rap1-knockout female mice displayed hearing loss phenotypically similar to AHL from an early age. The premature hearing loss in Cdk5rap1-knockout mice was associated with the degeneration of the spiral ligament and reduction of endocochlear potentials following the loss of auditory sensory cells. Furthermore, cultured primary mouse embryonic fibroblasts displayed early onset of cellular senescence associated with high oxidative stress and cell death. These results indicate that the CDK5RAP1 deficiency-induced defective mitochondrial translation might cause early hearing loss through the induction of cellular senescence and cochlear dysfunction in the inner ear. Our results suggest that the accumulation of dysfunctional mitochondria might promote AHL progression. Furthermore, our findings suggest that mitochondrial dysfunction and dysregulated mitochondrial tRNA modifications mechanistically cause AHL. Understanding the mechanisms underlying AHL will guide future clinical investigations and interventions in the attempt to mitigate the consequences of AHL.
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