Evidence map›Paper›PMID 35165294›Full record

ArticleCell death discovery2022

Downregulation of macrophage migration inhibitory factor attenuates NLRP3 inflammasome mediated pyroptosis in sepsis-induced AKI.

Tianlong Li, Haibin Sun, Yiming Li, Lianjiu Su, Jun Jiang, Ye Liu, Nanhui Jiang, Rong Huang, Jiahao Zhang, Zhiyong Peng

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 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
6.7field-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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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  17. [Electroacupuncture Alleviates Acute Kidney Injury in Septic Mice By Inhibiting the P2RX7/NLRP3 Signaling Pathway].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026
    Article
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15 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

10 authors at 1 institution in 2 countries.

Tianlong LiDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Haibin SunDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Yiming LiDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Lianjiu SuDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Jun JiangDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Ye LiuDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Nanhui JiangDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Rong HuangDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Jiahao ZhangDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China.
Zhiyong PengDepartment of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, Hubei province, 430071, China. zn001590@whu.edu.cn.ORCID http://orcid.org/0000-0002-0849-5648
Wuhan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81772046National Natural Science Foundation of China (National Science Foundation of China) 81971816
6 · The paper itself

Abstract

Sepsis-induced AKI (acute kidney injury) is considered an inflammation-related disease with high mortality. LPS-induced (Lipopolysaccharide) TLR4-NFκB pathway activation plays an important role in sepsis-induced AKI. Pyroptosis closely associated with inflammation response includes inflammasome formation, caspase1 activation and GSDMD N-terminal fragment cleavage that leads to cell membrane rupture and cell death, which may be related to the pathogenesis of sepsis-induced AKI. MIF (Macrophage migration inhibitory factor), associated with inflammation response, has been proved as a biomarker of sepsis, and perhaps regulate pyroptosis in sepsis-induced AKI. In this study, we focus on investigating the mechanism of MIF promoting pyroptosis in sepsis-induced AKI. MIF and pyroptosis-related proteins were up-regulated in kidney tissue of mice with CLP (cecum ligation puncture) surgery and in LPS-injured human kidney-2 (HK-2) cells. NLRP3 was down-regulated following the suppression of MIF topoisomerase activity by ISO-1 in kidney tissue of CLP mice. Knockdown of MIF alleviated NLRP3 inflammasome mediated pyroptosis in LPS-injured HK-2 cells. Meanwhile, we noted that phosphorylation of p65 was down-regulated by knockdown of MIF. Up-regulation of NLRP3 in response to LPS stimulation could be reversed by JSH-23, an inhibitor of NFκB pathway, but MIF was not affected. In conclusion, up-regulation of MIF in sepsis-induced AKI shows a renal damaged effect that aggravates NLRP3 inflammasome mediated cell pyroptosis through promoting phosphorylation of p65. This study demonstrated a novel mechanism of MIF regulating NLRP3 inflammasome mediated pyroptosis in sepsis-induced AKI.

Identifiers

PMID35165294
PMCPMC8844278
OpenAlexW4212921153

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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.