Evidence map›Paper›PMID 42045681›Full record

ArticleCell death and differentiation2026

NINJ1 ubiquitination by TRIM72 protects against plasma membrane rupture and AKI-CKD progression.

Keng Ye, Siyi Lin, Caiming Chen, Zhimin Chen, Kongwen Lin, Guoping Li, Huabin Ma, Jianfeng Wu, Tak W Mak, Li Chen and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026
    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

11 authors.

Keng Ye *Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID http://orcid.org/0000-0002-3661-3664
Siyi Lin *Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Caiming Chen *Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Zhimin ChenDepartment of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID http://orcid.org/0000-0002-4260-1774
Kongwen LinDepartment of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Guoping LiDepartment of Pathology, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID http://orcid.org/0000-0002-7662-6021
Huabin MaResearch Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID http://orcid.org/0000-0002-0581-4615
Jianfeng WuLaboratory Animal Research Center, Xiamen University, Xiamen, China.ORCID http://orcid.org/0000-0002-8992-2030
Tak W MakPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada. tmak@uhnres.utoronto.ca.
Li ChenResearch Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China. chenlify@fjmu.edu.cn.
Yanfang XuDepartment of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China. xuyanfang99@hotmail.com.ORCID http://orcid.org/0000-0002-6207-545X

Funding

National Natural Science Foundation of China (National Science Foundation of China) U23A20410
6 · The paper itself

Abstract

The progression of acute kidney injury (AKI) to chronic kidney disease (CKD) remains a major clinical challenge. It is primarily triggered by renal tubular epithelial cell (RTEC) death that leads to persistent sterile inflammation, maladaptive repair and irreversible renal fibrosis. A pivotal event in RTEC death is plasma membrane rupture (PMR), which leads to the release of Damage-Associated Molecular Patterns (DAMPs). In this study, we identified Tripartite Motif-Containing 72 (TRIM72) as a critical regulator of Ninjurin-1 (NINJ1), a key mediator of PMR. Using tubule-specific knockout mice (Ninj1

Identifiers

PMID42045681

What OpenQuestion holds

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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.