Evidence map›Paper›PMID 35449198›Full record

ArticleCell death discovery2022

Ferroptosis is involved in PGPS-induced otitis media in C57BL/6 mice.

Bin Yan, Daoli Xie, Yuancheng Wu, Shuli Wang, Xiaolin Zhang, Tong Zhao, Luying Liu, Peng Ma, Guqiang Li, Ying Yang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Ferroptosis and hearing loss: from molecular mechanisms to therapeutic interventions.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. 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

15 authors at 2 institutions in 2 countries.

Bin Yan *Hearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China.
Daoli Xie *Hearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China.
Yuancheng WuHearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China.
Shuli WangHearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China.
Xiaolin ZhangDepartment of Otolaryngology/Head and Neck Surgery, Institute of Otolaryngology, Affiliated Hospital of Binzhou Medical University, Binzhou, China.
Tong ZhaoHearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China.
Luying LiuDepartment of Pathology, School of Basic Medicine, Binzhou Medical University, Yantai, China.
Peng MaDepartment of Genetics, School of Basic Medicine, Binzhou Medical University, Yantai, China.
Guqiang LiRehabilitation Medicine & Physical Therapy, School of Rehabilitation Medicine, Binzhou Medical University, Yantai, China.
Ying YangHearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China.
Yucheng ZhaoHearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China.
Tihua ZhengHearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China.
Ruishuang GengHearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China. gengruishuang@hotmail.com.ORCID http://orcid.org/0000-0003-4363-3070
Bo LiHearing and Speech Rehabilitation Institute, College of Special Education, Binzhou Medical University, Yantai, China. liboyjt@163.com.ORCID http://orcid.org/0000-0002-5076-9614
Qingyin ZhengDepartment of Otolaryngology-Head & Neck Surgery, Case Western Reserve University, Cleveland, OH, USA.
Binzhou Medical University · CNCase Western Reserve University · US

Funding

Deciphering the Usher I protein interactome using a geneticapproachR01DC015111 · NIDCD · CASE WESTERN RESERVE UNIVERSITY · PI ZHENG, QING Y · 2016 to 2020
$1.8M
NIDCD NIH HHS R01 DC015111
6 · The paper itself

Abstract

Otitis media (OM) is a common disease that can cause hearing loss in children. Currently, the main clinical treatment for OM is antibiotics, but the overuse of antibiotics might lead to bacterial resistance, which is a worldwide public health challenge. Studying the pathogenesis of OM will help us develop new effective treatments. Ferroptosis is one type of programmed cell death characterized by the occurrence of lipid peroxidation driven by iron ions. Many studies have shown that ferroptosis is associated with infectious diseases. It is presently unclear whether ferroptosis is involved in the pathogenesis of OM. In this study, we explored the relationship between ferroptosis and OM by PGPS-induced OM in C57BL/6 mice and treating the induced OM with ferroptosis inhibitors deferoxamine (DFO), Ferrostatin-1 (Fer-1), and Liperoxstatin-1 (Lip-1). We examined the expression of ferroptosis-related proteins acyl-CoA synthetase long chain family member 4 (ACSL4) and prostaglandin-endoperoxide synthase 2 (Cox2), glutathione peroxidase 4 (GPX4) protein as well as lipid peroxidation markers 4-hydroxynonenal (4-HNE) and malondialdehyde (MDA). The results showed that in PGPS-induced OM model mice, several ferroptosis-related proteins including ACSL4 and Cox2 were up-regulated compared to mice treated with saline. Meanwhile, a ferroptosis-related protein GPX4 was down-regulated upon PGPS treatment. The DFO treatment in PGPS-inoculated mice effectively inhibited the development of OM. The inhibitors treatment caused a significant decrease in the expression of ACSL4, Cox2, 4 HNE, MDA, reduction in free iron. Meanwhile, the ferroptosis inhibitors treatment caused increase in the expression of inflammation-related factors tumor necrosis factor-α (TNF-α) and antioxidant protein GPX4. Our results suggest that there is a crosstalk between ferroptosis signaling pathway and the pathogenesis of OM. Ferroptosis inhibition can alleviate PGPS-induced OM.

Identifiers

PMID35449198
PMCPMC9023543
OpenAlexW4224248897

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Registered trials

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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.