Evidence map›Paper›PMID 35837696›Full record

ArticleRenal failure2022

Disulfiram ameliorates ischemia/reperfusion-induced acute kidney injury by suppressing the caspase-11-GSDMD pathway.

Qiaoting Cai, Zhaoxing Sun, Sujuan Xu, Xiaoyan Jiao, Shulan Guo, Yingxiang Li, Huan Wu, Xiaofang Yu

Open access · goldAbstract read
In one paragraph

Article in Renal failure, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Disulfiram Attenuates Adenine-Induced Renal Fibrosis by Modulating Inflammatory and Immunometabolic Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Myeloid Cells in Acute Kidney Injury.Seminars in nephrology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Can disulfiram modulate liver injury in CCl4-induced fibrosis in rats?Gastroenterology and hepatology from bed to bench · 2025
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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 4 institutions in 1 country.

Qiaoting CaiDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Zhaoxing SunDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Sujuan XuDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaoyan JiaoDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Shulan GuoDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Yingxiang LiDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Huan WuDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaofang YuDepartment of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Fudan University · CNShanghai Blood Center · CNZhongshan Hospital · CNShanghai Institute of Hematology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is a serious condition with high mortality. The most common cause is kidney ischemia/reperfusion (IR) injury, which is thought to be closely related to pyroptosis. Disulfiram is a well-known alcohol abuse drug, and recent studies have shown its ability to mitigate pyroptosis in mouse macrophages. This study investigated whether disulfiram could improve IR-induced AKI and elucidated the possible molecular mechanism. We generated an IR model in mouse kidneys and a hypoxia/reoxygenation (HR) injury model with murine tubular epithelial cells (MTECs). The results showed that IR caused renal dysfunction in mice and triggered pyroptosis in renal tubular epithelial cells, and disulfiram improved renal impairment after IR. The expression of proteins associated with the classical pyroptosis pathway (Nucleotide-binding oligomeric domain (NOD)-like receptor protein 3 (NLRP3), apoptosis-related specific protein (ASC), caspase-1, N-GSDMD) and nonclassical pyroptosis pathway (caspase-11, N-GSDMD) were upregulated after IR. Disulfiram blocked the upregulation of nonclassical but not all classical pyroptosis pathway proteins (NLRP3 and ASC), suggesting that disulfiram might reduce pyroptosis by inhibiting the caspase-11-GSDMD pathway.

Indexed as

Acute Kidney InjuryReperfusion InjuryAnimalsCaspasesComputer SimulationDisulfiramIschemiaKidneyMiceNLR Family, Pyrin Domain-Containing 3 ProteinReperfusionToll-Like Receptor 4CaspasesDisulfiramNLR Family, Pyrin Domain-Containing 3 ProteinToll-Like Receptor 4caspase-11disulfiramGSDMDKidney IR injurypyroptosis

Identifiers

PMID35837696
PMCPMC9291718
OpenAlexW4285585217

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.