Evidence map›Paper›PMID 42618924›Full record

ArticleJournal of biomedical science2026

NOX2 deficiency exacerbates lupus nephritis through activation of NLRP3 inflammasome in neutrophils.

Chun-Hsin Wu, Fang-Yu Lin, Miao-Shan Lin, Tzu-Yi Chan, Ying-Ren Chen, Hui-Ching Cheng, Chao-Kai Hsu, Chih-An Chen, Peng-Chieh Chen, Siao-Muk Cheng and 5 more

Abstract read
In one paragraph

Article in Journal of biomedical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Chun-Hsin WuInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, No. 35, Xiaodong Road, Tainan City, 704, Taiwan.
Fang-Yu LinInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, No. 35, Xiaodong Road, Tainan City, 704, Taiwan.
Miao-Shan LinInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, No. 35, Xiaodong Road, Tainan City, 704, Taiwan.
Tzu-Yi ChanInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, No. 35, Xiaodong Road, Tainan City, 704, Taiwan.
Ying-Ren ChenDepartment of Pathology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Hui-Ching ChengDepartment of Dermatology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chao-Kai HsuDepartment of Dermatology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chih-An ChenDepartment of Pediatrics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Peng-Chieh ChenInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, No. 35, Xiaodong Road, Tainan City, 704, Taiwan.
Siao-Muk ChengNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Daw-Yang HwangNational Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.
Junne-Ming SungDivision of Nephrology, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yau-Sheng TsaiInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, No. 35, Xiaodong Road, Tainan City, 704, Taiwan.
Pin LingDepartment of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chi-Chang ShiehInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, No. 35, Xiaodong Road, Tainan City, 704, Taiwan. cshieh@mail.ncku.edu.tw.

Funding

Ministry of Science and Technology, Taiwan MOST 110-2314-B-006-092-MY3National Cheng Kung University Hospital NCKUH-11302054
6 · The paper itself

Abstract

backgroundLupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE) associated with significant morbidity. Although reduced production of reactive oxygen species (ROS) by neutrophils correlates with severe SLE, the specific mechanisms linking ROS deficiency to heightened renal inflammation remain unknown. We aimed to elucidate the role of NOX2-derived ROS in LN pathogenesis and identify potential therapeutic targets.

methodsWe conducted an in vivo study using a pristane-induced lupus model in Ncf1

resultsNOX2 deficiency exacerbated LN severity compared to wild-type controls, demonstrated by increased serum anti-dsDNA antibody titers and worsened LN scores. Through scRNA-seq, we identified a distinct, activated neutrophil subset in Ncf1

conclusionOur results showed that NOX2 deficiency was associated with the expansion of a highly inflammatory renal neutrophil subset that may contribute to aggravated renal inflammation. These findings suggest that NOX2 functions as a negative regulator of the NLRP3 inflammasome and IL-1β blockade represents a promising precision therapeutic strategy for patients with LN who exhibit impaired ROS production.

Indexed as

InflammasomesLupus NephritisNADPH Oxidase 2NeutrophilsNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsDisease Models, AnimalFemaleMiceMice, KnockoutReactive Oxygen SpeciesCybb protein, mouseInflammasomesNADPH Oxidase 2NLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen SpeciesIL-1βLupus nephritisNeutrophilsNLRP3NOX2Reactive oxygen species

Identifiers

PMID42618924
PMCPMC13491832

What Socratic holds

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Registered trials

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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 Socratic graph.