Evidence map›Paper›PMID 37258461›Full record

ArticleFEBS open bio2023

Mitochondrial alterations in the cochlea of Cdk5rap1-knockout mice with age-related hearing loss.

Toru Miwa, Tatsuya Katsuno, Fan-Yan Wei, Kazuhito Tomizawa

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 24% of its field
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

5 citing papers in PubMed, 6 citations in OpenAlex.

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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

4 authors at 4 institutions in 2 countries.

Toru MiwaDepartment of Otolaryngology-Head and Neck Surgery, Graduate School of Medicine, Kyoto University, Japan.ORCID 0000-0002-5977-0056
Tatsuya KatsunoDepartment of Otolaryngology-Head and Neck Surgery, Osaka Metropolitan University, Japan.
Fan-Yan WeiDepartment of Molecular Physiology, Faculty of Life Sciences, Kumamoto University, Japan.ORCID 0000-0002-4843-724X
Kazuhito TomizawaDepartment of Molecular Physiology, Faculty of Life Sciences, Kumamoto University, Japan.ORCID 0000-0002-5663-2627
Kumamoto University · JPKyoto University · JPOsaka Metropolitan University · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have revealed that age-related hearing loss (AHL) in Cdk5 regulatory subunit-associated protein 1 (Cdk5rap1)-knockout mice is associated with pathology in the cochlea. Here, we aimed to identify mitochondrial alterations in the cochlea of Cdk5rap1-knockout mice with AHL. Mitochondria in the spiral ganglion neurons (SGNs) and hair cells (HCs) were normal despite senescence; however, the mitochondria of types I, II, and IV spiral ligament fibrocytes were ballooned, damaged, and ballooned, respectively, in the stria vascularis. Our results suggest that the accumulation of dysfunctional mitochondria in the lateral wall, rather than the loss of HCs and SGNs, leads to the onset of AHL. Our results provide valuable information regarding the underlying mechanisms of AHL and the relationship between aberrant tRNA modification-induced hearing loss and mitochondrial dysfunction.

Indexed as

CochleaHearing LossAnimalsMiceMice, KnockoutMitochondriaMitochondrial ProteinsPhosphotransferasesSulfur Group TransferasesCdk5r1 protein, mouseCdk5rap1 protein, mouseMitochondrial ProteinsPhosphotransferasesSulfur Group Transferasesage-related hearing lossCdk5rap1microstructural findingsmitochondriamitochondrial tRNAtransmission electron microscopy

Identifiers

PMID37258461
PMCPMC10315731
OpenAlexW4378904292

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.