Evidence map›Paper›PMID 39271015›Full record

ArticleCellular and molecular gastroenterology and hepatology2024

XBP1 Facilitating NF-κB-p65 Nuclear Translocation Promotes Macrophage-Originated Sterile Inflammation Via Regulating MT2 Transcription in the Ischemia/Reperfusion Liver.

Jianhua Rao, Zeng Wang, Fei Yu, Junda Li, Wenzhu Li, Zhengfeng Xuan, Yongquan Chi, Feng Zhang, Liming Tang, Feng Cheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. The IRE1Cell stress · 2026
    Article
  4. 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

10 authors.

Jianhua RaoHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China. Electronic address: raojh@njmu.edu.cn.
Zeng WangHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China; Center of Gastrointestinal Disease, The Affiliated Changzhou NO.2 People's Hospital of Nanjing Medical University, Changzhou, China.
Fei YuHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China.
Junda LiHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China.
Wenzhu LiHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China.
Zhengfeng XuanHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China.
Yongquan ChiHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China.
Feng ZhangHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China.
Liming TangCenter of Gastrointestinal Disease, The Affiliated Changzhou NO.2 People's Hospital of Nanjing Medical University, Changzhou, China. Electronic address: drtangliming@163.com.
Feng ChengHepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University, Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China. Electronic address: docchengfeng@njmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsXBP1, most conserved transcription factor of endoplasmic reticulum stress, plays important roles in physiological and pathologic settings and has profound effects on disease progression and prognosis, so it is necessary to investigate XBP1 in macrophage-originated sterile inflammation during liver ischemia/reperfusion injury (IRI). Macrophage XBP1 expression and liver injury are analyzed in patients undergoing ischemia-related hepatectomy.

methodsA myeloid-specific male XBP1-knockout (XBP1

resultsClinically, macrophage XBP1 expression significantly increases in ischemic liver tissues and positively correlates with liver injury after hepatectomy. Less hepatocellular damage is presented in XBP1

conclusionsXBP1 promotes macrophage-originated sterile inflammation, increases liver IRI by binding to MT2 promoter, and regulates MT2/nuclear factor-κB pathway, potentially therapeutic for clinical liver IRI.

Indexed as

LiverMacrophagesMice, KnockoutReperfusion InjuryTranscription Factor RelAX-Box Binding Protein 1AnimalsDisease Models, AnimalGene Expression RegulationHepatectomyHepatocytesHumansInflammationMaleMiceMice, Inbred C57BLTranscription Factor RelAX-Box Binding Protein 1XBP1 protein, humanXbp1 protein, mouseIschemia/Reperfusion InjuryMacrophagesMT2NF-κBXBP1

Identifiers

PMID39271015
PMCPMC11546936

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.