Evidence map›Paper›PMID 26319214›Full record

ArticleAging2015

Oxidative stress and ROS metabolism via down-regulation of sirtuin 3 expression in Cmah-null mice affect hearing loss.

Deug-Nam Kwon, Woo-Jin Park, Yun-Jung Choi, Sangiliyandi Gurunathan, Jin-Hoi Kim

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. The Role of Calcium Signaling in Sensorineural Hearing Loss.International journal of medical sciences · 2025
    Review
  3. Review
  4. Article
  5. Roles of Sirtuins in Hearing Protection.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  6. Article
  7. Review
  8. The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Mitochondrial Damage and Necroptosis in Aging Cochlea.International journal of molecular sciences · 2020
    Article
  17. Review
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Deug-Nam KwonDepartment of Animal Biotechnology, Konkuk University, Seoul 143-701, Republic of Korea.
Woo-Jin ParkDepartment of Animal Biotechnology, Konkuk University, Seoul 143-701, Republic of Korea.
Yun-Jung ChoiDepartment of Animal Biotechnology, Konkuk University, Seoul 143-701, Republic of Korea.
Sangiliyandi GurunathanDepartment of Animal Biotechnology, Konkuk University, Seoul 143-701, Republic of Korea.
Jin-Hoi KimDepartment of Animal Biotechnology, Konkuk University, Seoul 143-701, Republic of Korea.
Konkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CMP-Neu5Ac hydroxylase (Cmah) disruption caused several abnormalities and diseases including hearing loss in old age. However, underling molecular mechanisms that give rise to age-related hearing loss (AHL) in Cmah-null mouse are still obscure. In this study, Cmah-null mice showed age-related decline of hearing associated with loss of sensory hair cells, spiral ganglion neurons, and/or stria vascularis degeneration in the cochlea. To identify differential gene expression profiles and pathway associated with AHL, we performed microarray analysis using Illumina MouseRef-8 v2 Expression BeadChip and pathway-focused PCR array in the cochlear tissues of Cmah-null mouse. Pathway and molecular mechanism analysis using differentially expressed genes provided evidences that altered biological pathway due to oxidative damage by low expressed antioxidants and dysregulated reactive oxygen species (ROS) metabolism. Especially, low sirtuin 3 (Sirt3) gene expressions in Cmah-null mice decreased both of downstream regulator (Foxo1 and MnSod) and regulatory transcription factor (Hif1αand Foxo3α) gene expression. Taken together, we suggest that down-regulation of Sirt3 expression leads to oxidative stress and mitochondrial dysfunction by regulation of ROS and that it could alter various signaling pathways in Cmah-null mice with AHL.

Indexed as

AnimalsDisease Models, AnimalEar, InnerGene Expression ProfilingHearing LossMice, Inbred C57BLMitochondriaMixed Function OxygenasesOxidative StressReactive Oxygen SpeciesSirtuin 3Wnt Signaling PathwayCMPacetylneuraminate monooxygenaseMixed Function OxygenasesReactive Oxygen SpeciesSirt3 protein, mouseSirtuin 3CMP-N-acetylneuraminic acid hydroxylasehearing lossmitochondria dysfunctionoxidative stressROS metabolism

Identifiers

PMID26319214
PMCPMC4586103
OpenAlexW1232215139

What OpenQuestion holds

Textmetadata
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.