Evidence map›Paper›PMID 42571453›Full record

ArticleMilitary Medical Research2026

ZBP1 activated by mitochondrial damage binds to STAT3 to suppress Legumain production and exacerbate macrophage inflammation in

Li-Ting Deng, Huan Yang, Xu-Fei Zhang, Ze-Xing Lin, Ni Kuang, Hai-Yang Jiang, Pei-Zhao Liu, Yang-Guang Li, Xuan-Heng Li, Wei-Zhen Li and 9 more

Abstract read
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Article in Military Medical Research, 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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

19 authors.

Li-Ting DengSchool of Medicine, Southeast University, Nanjing 210009, China.
Huan YangDepartment of General Surgery, Clinical Translational Research Center for Surgical Infection and Immunity, the Affiliated BenQ Hospital of Nanjing Medical University, Nanjing 210026, China.
Xu-Fei ZhangDepartment of General Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210008, China.
Ze-Xing LinDepartment of General Surgery, Clinical Translational Research Center for Surgical Infection and Immunity, the Affiliated BenQ Hospital of Nanjing Medical University, Nanjing 210026, China.
Ni KuangDepartment of Infectious Diseases, Chongqing Key Laboratory for Research of Infectious Diseases, Southwest Hospital, Army Medical University, Chongqing 400038, China.
Hai-Yang JiangDepartment of General Surgery, Clinical Translational Research Center for Surgical Infection and Immunity, the Affiliated BenQ Hospital of Nanjing Medical University, Nanjing 210026, China.
Pei-Zhao LiuResearch Institute of General Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210002, China.
Yang-Guang LiResearch Institute of General Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210002, China.
Xuan-Heng LiResearch Institute of General Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210002, China.
Wei-Zhen LiResearch Institute of General Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210002, China.
Chu-Jun NiDepartment of General Surgery, Clinical Translational Research Center for Surgical Infection and Immunity, the Affiliated BenQ Hospital of Nanjing Medical University, Nanjing 210026, China.
Ming-Jie QiuResearch Institute of General Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210002, China.
Yue ChaoResearch Institute of General Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210002, China.
Yu-Fei PanSchool of Medicine, Southeast University, Nanjing 210009, China.
Yi-Yu YangSchool of Medicine, Southeast University, Nanjing 210009, China.
Ye-Ting ZhuResearch Institute of General Surgery, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210002, China.
Yun ZhaoDepartment of General Surgery, Clinical Translational Research Center for Surgical Infection and Immunity, the Affiliated BenQ Hospital of Nanjing Medical University, Nanjing 210026, China.
Jian-An RenSchool of Medicine, Southeast University, Nanjing 210009, China.
Xiu-Wen WuSchool of Medicine, Southeast University, Nanjing 210009, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Severe bacterial sepsis caused by Methods: To investigate the role of macrophage ZBP1 in sepsis, we combined transcriptomic datasets from human sepsis cohorts and murine sepsis and Results: ZBP1 activation was driven by both type I interferon (IFN-I) signaling and mitochondrial damage. Mechanistically, ZBP1 directly interacted with signal transducer and activator of transcription 3 (STAT3), suppressed its phosphorylation and nuclear translocation, and consequently inhibited transcription of Conclusion: These findings reveal a previously unrecognized ZBP1-STAT3-LGMN signaling axis that contributes to immune and inflammatory dysregulation in

Indexed as

Cysteine EndopeptidasesDNA-Binding ProteinsKlebsiella InfectionsMacrophagesMitochondriaRNA-Binding ProteinsSepsisSTAT3 Transcription FactorAnimalsDisease Models, AnimalHumansInflammationKlebsiella pneumoniaeMiceMice, KnockoutCysteine EndopeptidasesDNA-Binding ProteinsRNA-Binding ProteinsStat3 protein, mouseSTAT3 Transcription FactorZbp1 protein, mouseKlebsiella pneumoniae (KP)Legumain (LGMN)MacrophageSepsisSignal transducer and activator of transcription 3 (STAT3)Z-DNA binding protein 1 (ZBP1)

Identifiers

PMID42571453
PMCPMC13452355

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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.