Evidence map›Paper›PMID 42893454›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

HECTD1 Directs HIF-1α to Facilitate Intestinal Inflammation and Carcinogenesis via Promoting Th17 Differentiation and Glycolysis.

Shuiyu Xu, Qiaoqiao Han, Feixiang Wang, Yuerong Zhang, Haoran Feng, Kun Liu, Fang Xiu Luo, Fei Yuan, Xuesong Zhao, Xiaoyan Yu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Shuiyu Xu *Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qiaoqiao Han *Shanghai Institute of Immunology, Department of Immunology and Microbiology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0001-9664-6532
Feixiang Wang *Shanghai Institute of Immunology, Department of Immunology and Microbiology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuerong Zhang *Department of Laboratory Medicine, Institute of Laboratory Medicine, School of Medicine, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Haoran FengDepartment of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Kun LiuDepartment of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Fang Xiu LuoDepartment of Pathology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0003-3054-9478
Fei YuanDepartment of Pathology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xuesong ZhaoDepartment of Radiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaoyan YuShanghai Institute of Immunology, Department of Immunology and Microbiology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Haiyan HuangDepartment of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0009-0009-5484-0084
Qiang ZouShanghai Institute of Immunology, Department of Immunology and Microbiology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ren ZhaoDepartment of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0003-1978-5912

Funding

National Natural Science Foundation of China 82271766
6 · The paper itself

Abstract

Targeting glucose metabolism in Th17 cells may be beneficial for treating inflammatory bowel disease (IBD) and colitis-associated cancer (CAC), however, the molecular mechanisms orchestrating Th17 cell metabolism remain unclear. Here, we revealed that HECTD1 regulates IGF2BP3-dependent HIF-1α translation to promote Th17 cell glycolysis and differentiation and that HECTD1 expression correlates with IBD and CAC pathogenesis. T-cell-specific deletion of HECTD1 mitigated the severity of colitis and CAC in murine models. RNA-seq revealed enrichment of Th17 differentiation, glycolysis/gluconeogenesis, and HIF-1 signaling pathways among differentially expressed genes between HECTD1-sufficient and HECTD1-deficient CD4

Indexed as

colitis‐associated cancerglycolysisHECTD1inflammatory bowel diseaseTh17 cells

Identifiers

PMID42893454
PMCPMC13677005

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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.