Evidence map›Paper›PMID 35668064›Full record

ArticleCell death & disease2022

STAT6 inhibits ferroptosis and alleviates acute lung injury via regulating P53/SLC7A11 pathway.

Youjing Yang, Yu Ma, Qianmin Li, Yi Ling, Yujia Zhou, Kaimiao Chu, Lian Xue, Shasha Tao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
24.2field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 172 citations in OpenAlex.

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  14. S-palmitoylation in ferroptosis: molecular mechanisms, modulators, and interplay with autophagy.Apoptosis : an international journal on programmed cell death · 2026
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36 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Youjing Yang *Chongqing University Central Hospital&Chongqing Emergency Medical Center, No.1 Jiankang Road, Yuzhong District, Chongqing, 400014, China.
Yu Ma *Chongqing University Central Hospital&Chongqing Emergency Medical Center, No.1 Jiankang Road, Yuzhong District, Chongqing, 400014, China.
Qianmin LiSchool of Public Health, Medical College of Soochow University, 199 Ren'ai Road, Suzhou, 215123, China.
Yi LingSchool of Public Health, Medical College of Soochow University, 199 Ren'ai Road, Suzhou, 215123, China.
Yujia ZhouSchool of Public Health, Medical College of Soochow University, 199 Ren'ai Road, Suzhou, 215123, China.
Kaimiao ChuSchool of Public Health, Medical College of Soochow University, 199 Ren'ai Road, Suzhou, 215123, China.
Lian XueSchool of Public Health, Medical College of Soochow University, 199 Ren'ai Road, Suzhou, 215123, China.
Shasha TaoChongqing University Central Hospital&Chongqing Emergency Medical Center, No.1 Jiankang Road, Yuzhong District, Chongqing, 400014, China. sstao@suda.edu.cn.ORCID 0000-0002-6765-3829
Soochow University · CNChongqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Compelling evidences have revealed the emerging role of ferroptosis in the pathophysiological process of acute lung injury (ALI), but its modulation is not clear. Here, we identified that STAT6 acted as a critical regulator of epithelium ferroptosis during ALI. Firstly, STAT6 expression and activity were increased in the ALI mice models caused by crystalline silica (CS), LPS and X-ray exposure. Followed by confirming the contribution of ferroptosis in the above ALI with ferrostatin-1 and deferoxamine intervention, bioinformatic analyses revealed that STAT6 expression was negatively correlated with ferroptosis. Consistently, lung epithelium-specific depletion of STAT6 in mice or STAT6 knockdown in cultured epithelial cells exacerbated ferroptosis in the above ALI. While overexpression of STAT6 in lung epithelial cells attenuated the ferroptosis. Mechanistically, SLC7A11 is a typical ferroptosis-related gene and negatively regulated by P53. CREB-binding protein (CBP) is a critical acetyltransferase of P53 acetylation, showing valuable regulation on targets' transcription. Herein, we found that STAT6 negatively regulates ferroptosis through competitively binding with CBP, which inhibits P53 acetylation and transcriptionally restores SLC7A11 expression. Finally, pulmonary-specific STAT6 overexpression decreased the ferroptosis and attenuated CS and LPS induced lung injury. Our findings revealed that STAT6 is a pivotal regulator of ferroptosis, which may be a potential therapeutic target for the treatment of acute lung injury.

Indexed as

Acute Lung InjuryFerroptosisAnimalsLipopolysaccharidesMiceMice, Inbred C57BLNF-E2-Related Factor 2STAT6 Transcription FactorTumor Suppressor Protein p53LipopolysaccharidesNF-E2-Related Factor 2Stat6 protein, mouseSTAT6 Transcription FactorTumor Suppressor Protein p53

Identifiers

PMID35668064
PMCPMC9169029
OpenAlexW4281980293

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.