Evidence map›Paper›PMID 39809743›Full record

ArticleCell death & disease2025

RNF128 deficiency in macrophages promotes colonic inflammation by suppressing the autophagic degradation of S100A8.

Xianwen Ran, Yue Li, Yahui Ren, Weilong Chang, Rui Deng, Huifen Wang, Weiwei Zhu, Yize Zhang, Yudie Cai, Jia Hu and 2 more

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Frontiers in microbiology · 2026
    Article
  5. Review
  6. Review
  7. 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.

Xianwen Ran *Department of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Yue Li *Translational Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Yahui Ren *Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Weilong ChangDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Rui DengDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Huifen WangDepartment of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Weiwei ZhuDepartment of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Yize ZhangGene Hospital of Henan Province, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Yudie CaiDepartment of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Jia HuInstitute of Biology and Medicine, College of Life and Health Sciences, Wuhan University of Science and Technology, Wuhan, 430081, China. hujia123@wust.edu.cn.ORCID 0000-0003-2618-2079
Di WangDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. diwangwhuh@126.com.
Zhibo LiuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. lzl1041100271@163.com.ORCID 0000-0002-9641-3402

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81902923National Natural Science Foundation of China (National Science Foundation of China) 82373038Natural Science Foundation of Henan Province (Henan Province Natural Science Foundation) 242300421480
6 · The paper itself

Abstract

Macrophages play important roles in maintaining intestinal homeostasis and in the pathogenesis of inflammatory bowel diseases (IBDs). However, the underlying mechanisms that govern macrophage-mediated inflammation are still largely unknown. In this study, we report that RNF128 is downregulated in proinflammatory macrophages. RNF128 deficiency leads to elevated levels of effector cytokines in vitro and accelerates the progression of IBD in mouse models. Bone marrow transplantation experiments revealed that RNF128 deficiency in bone marrow cells contributes to the worsening of DSS-induced colitis. Mechanistically, RNF128 interacts with and destabilizes S100A8 by promoting its autophagic degradation, which is mediated by the cargo receptor Tollip. Moreover, the administration of an S100A8 neutralizing antibody mitigated the development of colitis and improved survival in DSS-treated Rnf128

Indexed as

AutophagyCalgranulin AColitisColonInflammationMacrophagesUbiquitin-Protein LigasesAnimalsDextran SulfateDisease Models, AnimalHumansIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLMice, KnockoutCalgranulin ADextran SulfateIntracellular Signaling Peptides and ProteinsS100a8 protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID39809743
PMCPMC11733159

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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.