Evidence map›Paper›PMID 25474306›Full record

ArticlePloS one2014

Aminoglycoside stress together with the 12S rRNA 1494C>T mutation leads to mitophagy.

Jialing Yu, Jing Zheng, Xiaoxu Zhao, Junxia Liu, Zhuochao Mao, Yining Ling, Danni Chen, Chao Chen, Lanlan Hui, Limei Cui and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Autophagy in Sensorineural Hearing Loss: Jekyll or Hyde?International journal of molecular sciences · 2026
    Review
  3. Article
  4. Mitochondrial tRNAAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Mitochondrial diseases caused by mtDNA mutations: a mini-review.Therapeutics and clinical risk management · 2018
    Review
  12. Article
  13. Article
  14. Article
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

13 authors at 1 institution in 1 country.

Jialing YuInstitute of Genetics, Zhejiang University, Hangzhou, China.
Jing ZhengInstitute of Genetics, Zhejiang University, Hangzhou, China.
Xiaoxu ZhaoInstitute of Genetics, Zhejiang University, Hangzhou, China.
Junxia LiuInstitute of Genetics, Zhejiang University, Hangzhou, China.
Zhuochao MaoSchool of Basic Medical Sciences, Zhejiang University, Hangzhou, China.
Yining LingSchool of Agriculture and Biotechonlogy, Zhejiang University, Hangzhou, China.
Danni ChenInstitute of Genetics, Zhejiang University, Hangzhou, China.
Chao ChenInstitute of Genetics, Zhejiang University, Hangzhou, China.
Lanlan HuiInstitute of Genetics, Zhejiang University, Hangzhou, China.
Limei CuiInstitute of Genetics, Zhejiang University, Hangzhou, China.
Ye ChenInstitute of Genetics, Zhejiang University, Hangzhou, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, China.
Pingping JiangInstitute of Genetics, Zhejiang University, Hangzhou, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, China.
Min-Xin GuanInstitute of Genetics, Zhejiang University, Hangzhou, China; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, China.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aminoglycosides as modifying factors modulated the phenotypic manifestation of mitochondrial rRNA mutations and the incomplete penetrance of hearing loss. In this report, using cybrids harboring the m.1494C>T mutation, we showed that gentamycin aggravated mitochondrial dysfunction in a combination of the m.1494C>T mutation. The m.1494C>T mutation was responsible for the dramatic reduction in three mtDNA-encoded proteins of H-strand, with the average of 39% reduction, except of the MT-ND6 protein, accompanied with 21% reduction of ATP production and increase in mitochondrial reactive oxygen species, compared with those of control cybrids. After exposure to gentamycin, 35% reduction of mitochondrial ATP production was observed in mutant cybrids with a marked decrease of the mitochondrial membrane potential. More excessive cellular reactive oxygen species was detected with stimulus of gentamycin than those in mutant cells. Under gentamycin and m.1494C>T stress together, more dysfunctional mitochondria were forced to fuse and exhibited mitophagy via up-regulated LC3-B, as a compensatory protective response to try to optimize mitochondrial function, rather than undergo apoptosis. These findings may provide valuable information to further understand of mechanistic link between mitochondrial rRNA mutation, toxicity of AGs and hearing loss.

Indexed as

Adenosine TriphosphateCase-Control StudiesCell LineEnergy MetabolismFemaleGentamicinsHumansMembrane Potential, MitochondrialMitochondriaMitochondrial ProteinsMitophagyOrganelle ShapePoint MutationReactive Oxygen SpeciesRNA, RibosomalStress, PhysiologicalAdenosine TriphosphateGentamicinsMitochondrial ProteinsReactive Oxygen SpeciesRNA, RibosomalRNA, ribosomal, 12S

Identifiers

PMID25474306
PMCPMC4256443
OpenAlexW2008224500

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.