Evidence map›Paper›PMID 27721494›Full record

ArticleScientific reports2016

NLRP3 inflammasome mediates contrast media-induced acute kidney injury by regulating cell apoptosis.

Jianxiao Shen, Ling Wang, Na Jiang, Shan Mou, Minfang Zhang, Leyi Gu, Xinghua Shao, Qin Wang, Chaojun Qi, Shu Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 79 citations in OpenAlex.

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  7. Dysregulation of SRSF3/International journal of biological sciences · 2025
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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

13 authors at 1 institution in 1 country.

Jianxiao ShenDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Ling WangDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Na JiangDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Shan MouDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Minfang ZhangDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Leyi GuDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Xinghua ShaoDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Qin WangDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Chaojun QiDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Shu LiDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Wanpeng WangDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Xiajing CheDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Zhaohui NiDepartment of Nephrology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 1630 Dong Fang Road, Shanghai, 200127, China.
Renji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iodinated contrast media serves as a direct causative factor of acute kidney injury (AKI) and is involved in the progression of cellular dysfunction and apoptosis. Emerging evidence indicates that NLRP3 inflammasome triggers inflammation, apoptosis and tissue injury during AKI. Nevertheless, the underlying renoprotection mechanism of NLRP3 inflammasome against contrast-induced AKI (CI-AKI) was still uncertain. This study investigated the role of NLRP3 inflammasome in CI-AKI both in vitro and in vivo. In HK-2 cells and unilateral nephrectomy model, NLRP3 and NLRP3 inflammasome member ASC were significantly augmented with the treatment of contrast media. Moreover, genetic disruption of NLRP3 notably reversed contrast-induced expression of apoptosis related proteins and secretion of proinflammatory factors, similarly to the effects of ASC deletion. Consistent with above results, absence of NLRP3 in mice undergoing unilateral nephrectomy also protected against contrast media-induced renal cells phenotypic alteration and cell apoptosis via modulating expression level of apoptotic proteins. Collectively, we demonstrated that NLRP3 inflammasome mediated CI-AKI through modulating the apoptotic pathway, which provided a potential therapeutic target for the treatment of contrast media induced acute kidney injury.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCARD Signaling Adaptor ProteinsCell LineContrast MediaDisease Models, AnimalHumansInflammasomesMiceNLR Family, Pyrin Domain-Containing 3 ProteinUp-RegulationCARD Signaling Adaptor ProteinsContrast MediaInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanPYCARD protein, human

Identifiers

PMID27721494
PMCPMC5056378
OpenAlexW2530041085

What OpenQuestion holds

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LicenceCC BY
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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.