Evidence map›Paper›PMID 38622688›Full record

ArticleMilitary Medical Research2024

Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis.

Kai-Wei Jia, Ren-Qi Yao, Yi-Wen Fan, Ding-Ji Zhang, Ye Zhou, Min-Jun Wang, Li-Yuan Zhang, Yue Dong, Zhi-Xuan Li, Su-Yuan Wang and 11 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Military Medical Research, 2024. 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
3.0field-weighted citation impact, top 8% 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, 13 citations in OpenAlex.

  1. The mCells · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Mitigation of Ferroptosis in Diabetic Kidney Disease Through Mesenchymal Stem Cell Intervention via the Smad2/3/METTL3/S1PR1 Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  8. Article
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  10. Article
  11. Review
  12. Review
  13. Article
  14. 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

21 authors at 3 institutions in 2 countries.

Kai-Wei Jia *National Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Ren-Qi Yao *Department of General Surgery, the First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Yi-Wen Fan *National Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Ding-Ji Zhang *National Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Ye Zhou *National Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Min-Jun Wang *National Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Li-Yuan ZhangNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Yue DongNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Zhi-Xuan LiNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Su-Yuan WangNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Mu WangNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Yun-Hui LiNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Lu-Xin ZhangNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Ting LeiNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Liang-Chen GuiNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Shan LuNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Ying-Yun YangCenter for Immunotherapy, Chinese Academy of Medical Sciences, Beijing, 100005, China.
Si-Xian WangNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Yi-Zhi YuNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China.
Yong-Ming YaoTranslational Medicine Research Center, Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital, Beijing, 100853, China. c_ff@sina.com.
Jin HouNational Key Laboratory of Medical Immunology & Institute of Immunology, Naval Medical University, Shanghai, 200433, China. houjin@immunol.org.ORCID 0000-0002-8670-517X
Second Military Medical University · CNChinese PLA General Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

the National Natural Science Foundation of China 92269204
6 · The paper itself

Abstract

backgroundLiver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family.

methodsThe expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58

resultsExcessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the m

conclusionsThis study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of m

Indexed as

FerroptosisReperfusion InjuryAnimalsDichlorodiphenyl DichloroethyleneHepatocytesInterferon-alphaMiceRNARNA HelicasesRNA, MessengerDhx58 protein, mouseDichlorodiphenyl DichloroethyleneIfna protein, mouseInterferon-alphaRNARNA HelicasesRNA, MessengerDExH-box helicase 58 (DHX58)Glutathione peroxidase 4 (GPX4)Ischemia/reperfusion (I/R)m6A modificationYT521-B homology domain containing 2 (YTHDC2)

Identifiers

PMID38622688
PMCPMC11017495
OpenAlexW4394816981

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.