Evidence map›Paper›PMID 35538041›Full record

ArticleActa biochimica et biophysica Sinica2022

LncRNA H19 inhibits oxidative stress injury of cochlear hair cells by regulating miR-653-5p/SIRT1 axis.

Wen Xie, Ting Shu, Haisen Peng, Jiali Liu, Chunhua Li, Meiqun Wang, Ping Wu, Yuehui Liu

Open access · diamondAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2022. 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
1.6field-weighted citation impact, top 16% 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, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Presbycusis: Pathology, Signal Pathways, and Therapeutic Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Roles of Sirtuins in Hearing Protection.Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  8. Unveiling a novelActa biochimica et biophysica Sinica · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. NcRNA: key and potential in hearing loss.Frontiers in neuroscience · 2023
    Review
  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

8 authors at 1 institution in 1 country.

Wen XieDepartment of Otolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Ting ShuMedical Imaging Center, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Haisen PengDepartment of Otolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Jiali LiuDepartment of Otolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Chunhua LiDepartment of Otolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Meiqun WangDepartment of Otolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Ping WuDepartment of Otolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Yuehui LiuDepartment of Otolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is one of the important mechanisms of inner ear cell damage, which can lead to age-related hearing loss (ARHL). LncRNA H19 is significantly downregulated in the cochlea of old mouse, however, the role of H19 in the development of ARHL remains unclear. In this study, we aim to investigate the expression and function of H19 in oxidative stress injury of cochlear hair cells induced by HO. RT-qPCR and western blot analysis confirms that HEI-OC1 cells stimulated with HO decreases the expressions of H19 and SIRT1, but increases the expression of miR-653-5p. Overexpression of H19 could increase cell viability, ATP level and mitochondrial membrane potential, but reduce mitochondrial ROS generation and cell apoptosis ratio in HO-stimulated HEI-OC1 cells. MiR-653-5p is a target of H19, which can bind to the 3'-UTR of SIRT1. H19 is found to regulate the expression of SIRT1 through miR-653-5p. Further experiments demonstrates that H19 regulates HEI-OC1 cell viability, ATP level, mitochondrial membrane potential, mitochondrial ROS generation, and cell apoptosis ratio via the miR-653-5p/SIRT1 axis. In conclusion, lncRNA H19 inhibits oxidative stress injury of cochlear hair cells via the miR-653-5p/SIRT1 axis.

Indexed as

Hair Cells, AuditoryMicroRNAsRNA, Long NoncodingSirtuin 1Adenosine TriphosphateAnimalsApoptosisMiceOxidative StressReactive Oxygen SpeciesAdenosine TriphosphateH19 long non-coding RNAMicroRNAsMIRN653 microRNA, mouseReactive Oxygen SpeciesRNA, Long NoncodingSirt1 protein, mouseSirtuin 1cochlear hair celllncRNA H19oxidative stressSIRT1

Identifiers

PMID35538041
PMCPMC9828013
OpenAlexW4214648942

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.