Evidence map›Paper›PMID 41392079›Full record

ArticleNature communications2025

Activation of the RSAD2-YTHDF1 axis in smooth muscle causes inflammatory bowel disease via intercellular mitochondrial transfer.

Wen-Di Zhang, Dan-Dan Zhang, Xu Wang, Chen-Yang Li, Fan-Qin Li, Xin-Long Liu, Shi-Zhen Zhang, Wei Sun, Li-Jing Li, Han-Bing Wang and 6 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Pooled it
  2. 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

16 authors.

Wen-Di Zhang *Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
Dan-Dan Zhang *Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
Xu Wang *Department of Pathology, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Chen-Yang LiDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Shijiazhuang, China.
Fan-Qin LiDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
Xin-Long LiuDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
Shi-Zhen ZhangDepartment of Cardiology, the Second Hospital of Hebei Medical University, Shijiazhuang, China.
Wei SunDepartment of Cardiology, the Second Hospital of Hebei Medical University, Shijiazhuang, China.
Li-Jing LiDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
Han-Bing WangDepartment of Gastrointestinal Surgery, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Peng KongDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
Xiao-Qin LiuDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
De-Min LiuDepartment of Cardiology, the Second Hospital of Hebei Medical University, Shijiazhuang, China.
Xiao-Lan ZhangDepartment of Gastroenterology, the Second Hospital of Hebei Medical University, Shijiazhuang, China.
Ya-Bin LiuDepartment of Gastrointestinal Surgery, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China. liuyabin@hebmu.edu.cn.
Mei HanDepartment of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China. hanmei@hebmu.edu.cn.ORCID http://orcid.org/0000-0002-5338-4875

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32371161National Natural Science Foundation of China (National Science Foundation of China) 82370474National Natural Science Foundation of China (National Science Foundation of China) 82400508
6 · The paper itself

Abstract

Colonic smooth muscle cell (CSMC) hypertrophy and hyperplasia have been described in both human ulcerative colitis (UC) and animal models. The deletion of smooth muscle (SM) 22α induces the phenotypic switching of SMCs. Here, we report that Sm22α-deficient mice develop spontaneous colitis, which is characterized by radical S-adenosyl-methionine domain-containing 2 (RSAD2)-driven mitochondrial dysfunction and inflammation in CSMCs and ferroptosis in the colonic mucosa. Mechanistically, RSAD2 mediates YTH m

Indexed as

Inflammatory Bowel DiseasesMitochondriaMuscle, SmoothRNA-Binding ProteinsAdenosineAnimalsColitis, UlcerativeColonDisease Models, AnimalDynaminsFemaleHumansIntestinal MucosaMaleMiceMice, Inbred C57BLAdenosineDnm1l protein, mouseDynaminsMicrofilament ProteinsMuscle ProteinsN-methyladenosineReactive Oxygen SpeciesRNA-Binding Proteinstransgelin

Identifiers

PMID41392079
PMCPMC12847955

What OpenQuestion holds

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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.