Evidence mapPaperPMID 40650658Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

ACSS2-Mediated Histone H4 Lysine 12 Crotonylation (H4K12cr) Alleviates Colitis via Enhancing Transcription of CLDN7.

Ming Yuan, Shaopeng Chen, Zhensen Lin, Runfeng Yu, Kang Chao, Shubiao Ye, Qing Li, Haoxian Ke, Chi Zhang, Junfeng Huang and 5 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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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

15 authors.

Ming YuanDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.ORCID https://orcid.org/0000-0003-2935-3320
Shaopeng ChenDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Zhensen LinDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Runfeng YuDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Kang ChaoGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Shubiao YeDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Qing LiGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Haoxian KeDepartment of Gastrointestinal Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510288, China.
Chi ZhangDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Junfeng HuangDepartment of Gastrointestinal Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510288, China.
Guanzhan LiangDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Tuo HuDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Xiang GaoGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Ping LanDepartment of General Surgery (Colorectal Surgery), The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510655, China.
Xianrui WuDepartment of Gastrointestinal Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong, 510288, China.ORCID https://orcid.org/0000-0002-4743-7133

Funding

Fundamental Research Funds for the Central Universities, Sun Yat-sen University 23qnpy147Fundamental Research Funds for the Central Universities, Sun Yat-sen University 23xkjc023Guangdong Basic and Applied Basic Research Foundation 2022A1515111043Guangdong Basic and Applied Basic Research Foundation 2024A1515012813Guangdong Basic and Applied Basic Research Foundation 2024A1515013072Guangzhou Basic and Applied Basic Research Foundation 2023A04J1820Jiangxi Provincial Natural Science Foundation 20242BAB25537Key Research and Development Program of Guangzhou 2024B03J0211National Key R&D Program of China 2022YFA1304000National Natural Science Foundation of China 82303928National Natural Science Foundation of China 82370675National Natural Science Foundation of China 82470570Shenzhen Medical Research Fund A2402002the "Jie Bang Gua Shuai" Program from The Sixth Affiliated Hospital, Sun Yat-sen University 2022JBGS01the National Key Clinical Disciplinethe program of Guangdong Provincial Clinical Research Center for Digestive Diseases 2020B1111170004the Starting Funding of Faculty from Sun Yat-sen University 2021276Xinjiang Uyghur Autonomous Regional Collaborative Innovation Special Project-Science and Technology Assistance to Xinjiang 2024E02063Xinjiang Uyghur Autonomous Regional Natural Science Foundation 2024D01C05
6 · The paper itself

Abstract

Histone lysine crotonylation (Kcr), a highly conserved posttranslational modification, plays critical roles in various biological processes. Nevertheless, the dynamic alterations and functions of histone Kcr in inflammatory bowel disease (IBD) remain poorly explored. Herein, a notable decrease of both Pan-Kcr and ACSS2 (acyl-CoA synthetase short-chain family member 2), the key enzyme for crotonyl-CoA generation, is revealed in inflamed intestinal epithelial cells. Genetic or pharmacological inhibition of ACSS2 dramatically impairs mouse intestinal barrier integrity and exacerbates colitis. Mechanistically, ACSS2-mediated histone H4 lysine 12 crotonylation (H4K12cr) upregulates CLDN7 expression to fortify intestinal epithelial barrier, which can be augmented by crotonate supplementation. Furthermore, tumor necrosis factor-α (TNF-α) is revealed to enhance the m6A modification of ACSS2 mRNA, consequently destabilizing and downregulating ACSS2. Combinational therapy involving anti-TNF-α and crotonate can significantly ameliorate colitis. Overall, ACSS2-mediated H4K12cr emerges as a pivotal modulator governing intestinal barrier function during IBD progression.

Indexed as

ClaudinsColitisHistonesAnimalsDisease Models, AnimalHumansIntestinal MucosaLysineMaleMiceMice, Inbred C57BLProtein Processing, Post-TranslationalTumor Necrosis Factor-alphaClaudinsHistonesLysineTumor Necrosis Factor-alphaACSS2histone lysine crotonylationinflammatory bowel diseaseintestinal barrier

Identifiers

PMID40650658
PMCPMC12376547

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.