Evidence map›Paper›PMID 41390757›Full record

ArticleCell death discovery2025

Caspase 6 deficiency exacerbates inflammatory bowel disease via enterocyte necroptosis and bacterial translocation.

Qiong Liu, Jun He, Lixin Liu, Leping Yang, Xiaoyan Qi, Zuxing Wei, Xuyang Hou, Dekun Liu, Yimiao Cheng, Ganglei Liu and 2 more

Abstract read
In one paragraph

Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Qiong LiuDepartment of Stomatology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jun HeDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Lixin LiuDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Leping YangDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xiaoyan QiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zuxing WeiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xuyang HouDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Dekun LiuDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yimiao ChengDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Ganglei LiuDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Yanwen ZhengDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. zyw.1018@csu.edu.cn.
Kuijie LiuDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. liukuijie@csu.edu.cn.ORCID http://orcid.org/0000-0002-9628-6116

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caspase 6 is a pivotal executioner caspase involved in cell death; however, its role in inflammatory bowel disease (IBD) remains incompletely understood. Levels of cleaved caspase 6 were quantified in colonic tissues from IBD patients, and an IBD mouse model was established via DSS induction, incorporating both systemic (Casp6 KO) and IEC-specific knockout (Casp6 cKO) strategies. Single-cell RNA sequencing (scRNA-seq) revealed that Casp6 KO enhanced necroptosis in IECs, reducing intestinal endocrine cells and damaging intestinal stem cells. Both in vivo and in vitro studies confirmed that caspase 6 deficiency activates the necroptosis pathway by upregulating RIPK1 in IECs and impairs macrophage bacterial clearance. Importantly, Casp6 KO reduces bactericidal activity in a cathepsin L (CTSL)-dependent manner. These findings demonstrate that preserving caspase 6 activity is essential for necroptosis prevention and effective bacterial clearance, providing new insights for future IBD therapies.

Identifiers

PMID41390757
PMCPMC12848308

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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.