Evidence map›Paper›PMID 42350381›Full record

ArticleCell death & disease2026

NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury.

Wen-Jing Zhong, Yu-Biao Liu, Xin-Yu Yang, Meng-Rui Chen, Nan-Shi-Yu Yang, Chen-Yu Zhang, Jian-Bing Xiong, Wei-Feng Tang, Cha-Xiang Guan, Yan-Feng Zhang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 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

12 authors.

Wen-Jing ZhongDepartment of Geriatric Respiratory and Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yu-Biao LiuDepartment of Physiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Xin-Yu YangDepartment of Physiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Meng-Rui ChenDepartment of Physiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Nan-Shi-Yu YangDepartment of Physiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Chen-Yu ZhangDepartment of Physiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Jian-Bing XiongNational Clinical Research Center of Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Wei-Feng TangDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Cha-Xiang GuanDepartment of Physiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.ORCID http://orcid.org/0000-0002-8505-8724
Yan-Feng ZhangDepartment of Geriatric Respiratory and Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jia-Xi DuanDepartment of Geriatric Respiratory and Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, China. duanjiaxi91@csu.edu.cn.
Yong ZhouDepartment of Physiology, Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China. zhouyong421@csu.edu.cn.ORCID http://orcid.org/0000-0002-7348-2376

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82370086National Natural Science Foundation of China (National Science Foundation of China) 82400108
6 · The paper itself

Abstract

Excessive neutrophil extracellular traps (NETs) formation is a significant contributor to acute lung injury (ALI), making its inhibition a novel therapeutic avenue to improve outcomes. In this study, we revealed that a novel pore-forming protein ninjurin-1 (NINJ1) was highly expressed in pro-inflammatory neutrophil subpopulations during ALI, using public single-cell RNA sequencing and hotspot analysis. Furthermore, we demonstrated that the NINJ1 oligomerization was essential for the NET release in neutrophils from both acute respiratory distress syndrome (ARDS) patients and ALI mice. Genetic ablation of Ninj1 in neutrophils abolished NET release, thereby attenuating pulmonary dysfunction and reducing ALI-related lethality. Mechanistically, we found that K45 and N60 are critical for NINJ1 oligomerization and subsequent NET release. In summary, our findings reveal a novel pore-forming protein-mediated mechanism for NET release and highlight NINJ1 as a potential therapeutic target for the treatment of ALI/ARDS. Schematic illustration. The novel pore-forming protein NINJ1 mediates the extrusion of NETs, thereby exacerbating pulmonary injury in ARDS/ALI. K45 and N60 are essential for NINJ1 oligomerization and subsequent NET release.

Indexed as

Acute Lung InjuryCell Adhesion Molecules, NeuronalExtracellular TrapsNerve Growth FactorsNeutrophilsAnimalsHumansMaleMiceMice, Inbred C57BLRespiratory Distress SyndromeCell Adhesion Molecules, NeuronalNerve Growth FactorsNINJ1 protein, humanNinj1 protein, mouse

Identifiers

PMID42350381
PMCPMC13558649

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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.