Evidence map›Paper›PMID 36891515›Full record

ReviewFrontiers in cell and developmental biology2023

Mitochondrial dysfunction in hearing loss: Oxidative stress, autophagy and NLRP3 inflammasome.

Peipei Li, Shen Li, Le Wang, Hongmin Li, Yang Wang, Hongbing Liu, Xin Wang, Xiaodan Zhu, Zhangsuo Liu, Fanglei Ye and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Review
  3. Molecules (Basel, Switzerland) · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Autophagy in Sensorineural Hearing Loss: Jekyll or Hyde?International journal of molecular sciences · 2026
    Review
  10. Article
  11. Therapeutic Potential of MgHNeuroscience bulletin · 2026
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 2 institutions in 1 country.

Peipei LiDepartment of Integrated Traditional and Western Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Shen LiDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Le WangDepartment of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Hongmin LiDepartment of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yang WangDepartment of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Hongbing LiuDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xin WangDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xiaodan ZhuDepartment of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Zhangsuo LiuDepartment of Integrated Traditional and Western Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Fanglei YeDepartment of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yuan ZhangDepartment of Otology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CNHenan Provincial Center for Disease Control and Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sensorineural deafness becomes an inevitable worldwide healthy problem, yet the current curative therapy is limited. Emerging evidences demonstrate mitochondrial dysfunction plays a vital role of in the pathogenesis of deafness. Reactive oxygen species (ROS)-induced mitochondrial dysfunction combined with NLRP3 inflammasome activation is involved in cochlear damage. Autophagy not only clears up undesired proteins and damaged mitochondria (mitophagy), but also eliminate excessive ROS. Appropriate enhancement of autophagy can reduce oxidative stress, inhibit cell apoptosis, and protect auditory cells. In addition, we further discuss the interplays linking ROS generation, NLRP3 inflammasome activation, and autophagy underlying the pathogenesis of deafness, including ototoxic drugs-, noise- and aging-related hearing loss.

Indexed as

autophagyhearing lossmitochondrial dysfunctionNLRP3 inflammasomeoxidative stress

Identifiers

PMID36891515
PMCPMC9986271
OpenAlexW4321377450

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.