Evidence map›Paper›PMID 34642298›Full record

ArticleCell death & disease2021

Metformin alleviates inflammation through suppressing FASN-dependent palmitoylation of Akt.

Wenfang Xiong, Kuo-Yang Sun, Yan Zhu, Xiaoqi Zhang, Yi-Hua Zhou, Xiaoping Zou

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  7. The Roles of ProteinCancer communications (London, England) · 2026
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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

6 authors at 1 institution in 1 country.

Wenfang Xiong *Department of Gastroenterology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, PR China.
Kuo-Yang Sun *State Key Laboratory of Pharmaceutical Biotechnology, Department of Sports Medicine and Adult Reconstructive Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, PR China.
Yan ZhuDepartment of Gastroenterology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, PR China.
Xiaoqi ZhangDepartment of Gastroenterology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, PR China. 13770654281@163.com.
Yi-Hua ZhouDepartments of Laboratory Medicine and Infectious Diseases, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, PR China. zgr03summer@126.com.
Xiaoping ZouDepartment of Gastroenterology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, PR China. zouxp@nju.edu.cn.ORCID 0000-0003-4147-7051
Nanjing Drum Tower Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) No.81871947Six Talent Peaks Project in Jiangsu Province (Six Talent Peaks Project in Jiangsu Province of China) WSW-134
6 · The paper itself

Abstract

Metformin, traditionally regarded as a hypoglycemic drug, has been studied in other various fields including inflammation. The specific mechanism of metformin's effect on immune cells remains unclear. Herein, it is verified that LPS-induced macrophages are characterized by enhanced endogenous fatty acid synthesis and the inhibition of fatty acid synthase (FASN) downregulates proinflammatory responses. We further show that metformin could suppress such elevation of FASN as well as proinflammatory activation in macrophages. In vivo, metformin treatment ameliorates dextran sulfate sodium (DSS)-induced colitis through impairing proinflammatory activation of colonic lamina propria mononuclear cells (LPMCs). The reduction of FASN by metformin hinders Akt palmitoylation, which further disturbs Akt membrane attachment and its phosphorylation. Metformin-mediated suppression of FASN/Akt pathway and its downstream MAPK signaling contributes to its anti-inflammatory role in macrophages. From the perspective of immunometabolism, our work points towards metformin utilization as an effective and potential intervention against macrophages-involved inflammatory diseases.

Indexed as

Lipoylation4-ButyrolactoneAnimalsCell MembraneColitisDextran SulfateDown-RegulationEnzyme ActivationFatty Acid SynthasesInflammationIntestinal MucosaLipopolysaccharidesMacrophagesMaleMetforminMice2-bromopalmitate4-Butyrolactone4-methylene-2-octyl-5-oxofuran-3-carboxylic acidDextran SulfateFatty Acid SynthasesLipopolysaccharidesMetforminPalmitatesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTranscription Factor RelA

Identifiers

PMID34642298
PMCPMC8511025
OpenAlexW3205057133

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.