Evidence map›Paper›PMID 40801087›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025

ATF6 Alleviates Endothelial Inflammation Following Extended Hepatectomy Through Inhibition of TRIM10/NF-κB Signaling.

Cheng-Cheng Shi, Dong-Jing Yang, Yang Bai, Binhui Zhou, Yao-Hui Sun, Xiao-Ran Xu, Wen-Zhi Guo, Shui-Jun Zhang, Yinming Liang, Yang Jin and 1 more

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. ATF6 Alleviates Endothelial Inflammation Following Extended Hepatectomy Through Inhibition of TRIM10/NF-κB Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    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

11 authors.

Cheng-Cheng ShiDepartment of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China.
Dong-Jing YangDepartment of Hepatobiliary and Pancreatic Surgery, Henan Key Laboratory of Digestive Organ Transplantation & Zhengzhou Key Laboratory for HPB Diseases and Organ Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yang BaiDepartment of Hepatobiliary and Pancreatic Surgery, Henan Key Laboratory of Digestive Organ Transplantation & Zhengzhou Key Laboratory for HPB Diseases and Organ Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Binhui ZhouLaboratory of Genetic Regulators in the Immune System, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
Yao-Hui SunDepartment of Hepatobiliary and Pancreatic Surgery, Henan Key Laboratory of Digestive Organ Transplantation & Zhengzhou Key Laboratory for HPB Diseases and Organ Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xiao-Ran XuThe First Clinical School of Medicine of Zhengzhou University, Zhengzhou, China.
Wen-Zhi GuoDepartment of Hepatobiliary and Pancreatic Surgery, Henan Key Laboratory of Digestive Organ Transplantation & Zhengzhou Key Laboratory for HPB Diseases and Organ Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Shui-Jun ZhangDepartment of Hepatobiliary and Pancreatic Surgery, Henan Key Laboratory of Digestive Organ Transplantation & Zhengzhou Key Laboratory for HPB Diseases and Organ Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yinming LiangLaboratory of Genetic Regulators in the Immune System, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
Yang JinDepartment of Hepatobiliary and Pancreatic Surgery, Henan Key Laboratory of Digestive Organ Transplantation & Zhengzhou Key Laboratory for HPB Diseases and Organ Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Ji-Hua ShiDepartment of Hepatobiliary and Pancreatic Surgery, Henan Key Laboratory of Digestive Organ Transplantation & Zhengzhou Key Laboratory for HPB Diseases and Organ Transplantation, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID https://orcid.org/0000-0002-9267-7523

Funding

the Henan Program for Science and Technology Develpment, China 242102310232the Medical Science and Technology Program of Henan, China SBGJ202302055the Medical Science and Technology Program of Henan, China YXKC2022059the National Natural Science Foundation of China 81972752the National Natural Science Foundation of China 82204521
6 · The paper itself

Abstract

The inflammatory response in liver sinusoidal endothelial cells (LSECs) is crucial to the pathophysiology of postoperative hepatic failure. The unfolded protein response (UPR) in LSECs following surgical stress exerts an important mechanism for resolving endothelial inflammation and re-establishing liver homeostasis. We employed 80% hepatectomy in mice to simulate extended hepatectomy and verified the gene expression in the patients who underwent marginal hepatectomy. The UPR in LSECs and endothelial inflammation were induced with tunicamycin or lipopolysaccharides in HUVECs to investigate the expression, effect, and regulation of activating transcription factor 6 (ATF6) in endothelial inflammation. We found that UPR protein ATF6 in LSECs was upregulated and activated following extended hepatectomy in both mice and humans; ATF6 deficiency in mice by either global knockout or LSECs-specific knockdown failed to alleviate the inflammatory response and led to severe liver injury; genetic knockout or pharmacological inhibition of ATF6 by the ATF6 antagonist Ceapin-A7 in HUVECs led to severe inflammation through the nuclear factor-κB (NF-κB) signaling pathway, while the ATF6 agonist AA147 ameliorated inflammation. Mechanistically, ATF6 induced negative transcriptional control of tripartite motif-containing protein 10 (TRIM10) and the downstream NF-κB signaling pathway, thereby suppressing endothelial inflammation. Taken together, our data identify ATF6 as a suppressor of endothelial inflammation following extended hepatectomy and clarify the underlying regulatory mechanism of the ATF6-TRIM10/NF-κB signaling pathway. These findings highlight its potential as a therapeutic target for postoperative hepatic failure.

Indexed as

Activating Transcription Factor 6Endothelial CellsHepatectomyInflammationNF-kappa BUbiquitin-Protein LigasesAnimalsHumansHuman Umbilical Vein Endothelial CellsLiverMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionUnfolded Protein ResponseActivating Transcription Factor 6ATF6 protein, humanAtf6 protein, mouseNF-kappa BUbiquitin-Protein Ligasesliver sinusoidal endothelial cellpostoperative hepatic failuretripartite motif‐containing protein 10unfolded protein response activating transcription factor 6

Identifiers

PMID40801087
PMCPMC12344622

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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.