Evidence map›Paper›PMID 41618391›Full record

ArticleRespiratory research2026

Peroxiredoxin 1 mediates bleomycin-induced acute lung injury in mice via macrophage NOD1/NF-κB axis.

Guoliang Jiang, Yan Zhang, Lingzhi Long, Xiangyu Zhang, Tingting Yao, Xiaoyun Cheng, Pan Yu, Lijun Zou, Yijun He, Mao Jiang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 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. Article
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.

Guoliang JiangDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Yan ZhangHunan Key Laboratory of Organ Fibrosis, Central South University, Changsha, China.
Lingzhi LongDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Xiangyu ZhangDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Tingting YaoDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Xiaoyun ChengDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Pan YuDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Lijun ZouDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Yijun HeDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Mao JiangDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Qingxiang LiuDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China.
Jie MengDepartment of Respiratory and Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha, China. mengjie@csu.edu.cn.

Funding

National Natural Science Foundation of China 82270079National Natural Science Foundation of China 82300096
6 · The paper itself

Abstract

backgroundBleomycin (BLM), a widely used antitumor drug, has been demonstrated to induce pulmonary toxicity in both chemotherapy patients and experimental animals, leading to acute lung injury (ALI). However, the lack of effective treatment options limits its clinical application. While peroxiredoxin 1 (Prdx1), a novel damage-associated molecular pattern (DAMP), has been shown to exacerbate acute liver and kidney injury by promoting inflammatory responses, its role in BLM-induced ALI remains unclear.

methodsAn ALI mouse model was established via intratracheal instillation of BLM (5 mg/kg). Prdx1 gene-knockout mice, recombinant murine Prdx1 protein (rPrdx1), and Prdx1-neutralizing monoclonal antibody were utilized to investigate the role of Prdx1 in BLM-induced ALI. Further mechanistic insights were explored through single-cell RNA sequencing analysis.

resultsBLM-induced damage to bronchial epithelial cells triggered Prdx1 release, which subsequently activated the NOD1/NF-κB signaling pathway in macrophages, promoting the release of inflammatory cytokines and exacerbating pulmonary inflammation and pathological damage. These findings were confirmed by single-cell RNA sequencing. Genetic knockout of Prdx1 or administration of Prdx1-neutralizing monoclonal antibody protected mice from BLM-induced ALI, and this protective effect was attenuated by introducing rPrdx1.

conclusionThese findings identify Prdx1 as a potential therapeutic target for BLM-induced ALI, offering a strategy to mitigate its pulmonary toxicity and facilitate the broader clinical application of BLM.

Indexed as

Acute Lung InjuryBleomycinMacrophagesNF-kappa BNod1 Signaling Adaptor ProteinPeroxiredoxinsAnimalsAntibiotics, AntineoplasticMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionAntibiotics, AntineoplasticBleomycinNF-kappa BNod1 Signaling Adaptor ProteinPeroxiredoxinsPrdx1 protein, mouseAcute lung inguryBleomycinDAMPsMacrophageNOD1/NF-kB pathwayPeroxiredoxin 1

Identifiers

PMID41618391
PMCPMC12930967

What OpenQuestion 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 OpenQuestion graph.