Evidence map›Paper›PMID 40260078›Full record

ArticleFrontiers in cellular neuroscience2025

Mitochonic acid 5 mitigates age-related hearing loss progression by targeting defective 2-methylthiolation in mitochondrial transfer RNAs.

Teppei Kouga, Toru Miwa, Fan-Yan Wei, Kishiko Sunami, Kazuhito Tomizawa

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cellular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Teppei Kouga *Department of Otolaryngology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Toru Miwa *Department of Otolaryngology-Head and Neck Surgery, Kyoto University, Kyoto, Japan.
Fan-Yan WeiDepartment of Modomics Biology and Medicine, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
Kishiko SunamiDepartment of Otolaryngology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Kazuhito TomizawaDepartment of Molecular Physiology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Age-related hearing loss (ARHL) is linked to dementia, with mitochondrial dysfunction playing a key role in its progression. Deficient mitochondrial tRNA modifications impair protein synthesis and energy metabolism, accelerating ARHL. Mitochonic acid 5 (MA-5) has shown promise as a therapeutic candidate by improving mitochondrial function, reducing oxidative stress, and stabilizing membrane potential. Methods: In this study, we investigated the effects of MA-5 on ARHL in cyclin-dependent kinase 5 regulatory subunit-associated protein 1 ( Results: MA-5 treatment effectively attenuated ARHL progression in Conclusion: These findings suggest that MA-5 is a viable treatment option for ARHL and other age-related disorders associated with mitochondrial dysfunction.

Indexed as

2-methylthiolationage-related hearing losscyclin-dependent kinase 5 regulatory subunit-associated protein 1mitochondrial dysfunctionmitochonic acid 5

Identifiers

PMID40260078
PMCPMC12009901

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.