Evidence map›Paper›PMID 38233383›Full record

ArticleCell death & disease2024

Dietary long-chain fatty acids promote colitis by regulating palmitoylation of STAT3 through CD36-mediated endocytosis.

Yuping Wei, Jinting Li, Jiao Li, Chuan Liu, Xingzhou Guo, Zhengru Liu, Luyun Zhang, Shenglan Bao, Xiaohan Wu, Wenhao Su and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
16.6field-weighted citation impact, top 1% of its field
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

31 citing papers in PubMed, 29 citations in OpenAlex.

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  17. Gut microbes · 2025
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  19. Connecting the Dots: Stress Granule and Cardiovascular Diseases.Journal of cardiovascular translational research · 2025
    Review
  20. 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

13 authors at 3 institutions in 1 country.

Yuping Wei *Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.ORCID 0009-0006-6635-0179
Jinting Li *Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Jiao Li *Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Chuan Liu *Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Xingzhou GuoDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Zhengru LiuKey Laboratory of Hubei Province for Digestive System Disease, Wuhan, Hubei Province, China.
Luyun ZhangDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Shenglan BaoDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Xiaohan WuKey Laboratory of Hubei Province for Digestive System Disease, Wuhan, Hubei Province, China.
Wenhao SuDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
Xiaoli WangDepartment of Plastic Surgery, Renmin hospital of Wuhan University, Wuhan, Hubei Province, China.
Jixiang ZhangDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China. zhangjixiang@whu.edu.cn.ORCID 0000-0002-3742-8057
Weiguo DongDepartment of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China. dongweiguo@whu.edu.cn.ORCID 0000-0002-4228-6508
Wuhan University · CNChina Medical University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Western diet, characterized by its high content of long-chain fatty acids (LCFAs), is widely recognized as a significant triggering factor for inflammatory bowel disease (IBD). While the link between a high-fat diet and colitis has been observed, the specific effects and mechanisms remain incompletely understood. Our study provides evidence that the diet rich in LCFAs can disrupt the integrity of the intestinal barrier and exacerbate experimental colitis in mice. Mechanistically, LCFAs upregulate the signal transducer and activator of transcription-3 (STAT3) pathway in the inflammatory model, and STAT3 knockout effectively counters the pro-inflammatory effects of LCFAs on colitis. Specifically, palmitic acid (PA), a representative LCFA, enters intestinal epithelial cells via the cluster of differentiation 36 (CD36) pathway and participates in the palmitoylation cycle of STAT3. Inhibiting this cycle using pharmacological inhibitors like 2-Bromopalmitate (2-BP) and ML349, as well as DHHC7 knockdown, has the ability to alleviate inflammation induced by PA. These findings highlight the significant role of dietary LCFAs, especially PA, in the development and progression of IBD. Diet adjustments and targeted modulation offer potential therapeutic strategies for managing this condition. Model of LCFAs involvement in the palmitoylation cycle of STAT3 upon internalization into cells. Following cellular uptake through CD36, LCFAs are converted to palmitoyl-CoA. In the presence of DHHC7, palmitoyl-CoA binds to STAT3 at the C108 site, forming palmitoylated STAT3. Palmitoylation further promotes phosphorylation at the Y705 site of STAT3. Subsequently, palmitoylated STAT3 undergoes depalmitoylation by APT2 and translocates to the nucleus to exert its biological functions.

Indexed as

ColitisInflammatory Bowel DiseasesAnimalsDiet, High-FatEndocytosisFatty AcidsLipoylationMiceSTAT3 Transcription FactorFatty AcidsStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID38233383
PMCPMC10794235
OpenAlexW4390954602

What OpenQuestion holds

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LicenceCC BY
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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.