Evidence map›Paper›PMID 42618739›Full record

ArticleNature metabolism2026

Intestinal cGAS-STING-IFN signalling promotes obesity by downregulating microbiota-derived IAA in male mice.

Jiangming Deng, Wen Meng, Yuanqin Yang, Ting Xiao, Zhangliu Jin, Jing Wang, Qing-Xin Li, Lingxiang Xie, Jingyi Hu, Rong Song and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature metabolism, 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

18 authors.

Jiangming Deng *National Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.
Wen Meng *National Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.ORCID http://orcid.org/0000-0001-6785-0390
Yuanqin YangNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.
Ting XiaoThe Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, China.
Zhangliu JinThe Metabolic Syndrome Research Center, The Second Xiangya Hospital of Central South University, Changsha, China.
Jing WangNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.
Qing-Xin LiNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.
Lingxiang XieNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.
Jingyi HuNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.
Rong SongNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.
Yibo HuNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China.
Yi ChuDepartment of Gastroenterology, The Second Xiangya Hospital of Central South University, Changsha, China.
Qing LiDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, P. R. China.ORCID http://orcid.org/0000-0002-1787-4180
Ping JinDepartment of Endocrinology, The Third Xiangya Hospital of Central South University, Changsha, China.
Zheng WangCollege of Bioscience & Biotechnology of Hunan Agricultural University, Changsha, China.
Irene Xy WuDepartment of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, China.
Feng LiuNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China. liuf001@csu.edu.cn.ORCID http://orcid.org/0000-0002-5098-1711
Yang XiaoNational Clinical Research Center for Endocrine and Metabolic Diseases, Changsha, China. xiaoyang29@csu.edu.cn.ORCID http://orcid.org/0000-0003-3927-1839

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82330025
6 · The paper itself

Abstract

The gut constantly interacts with both pathogens and dietary signals, but how it balances immune and metabolic responses remains unclear. Here we show that intestinal cGAS, a key DNA sensor, acts as a regulator linking gut immunity to whole-body metabolism. We show that cGAS signalling is activated in the intestines of humans and male mice with obesity, leading to increased type I interferon production and heightened immune activity in intestinal cells. Strikingly, deleting cGAS specifically in intestinal epithelial cells enhances energy expenditure, protects against diet-induced obesity and improves metabolic health. These effects depend on the gut microbiota, particularly Lactobacillus murinus and its metabolite indole-3-acetic acid (IAA), which promotes adipose thermogenesis. Our findings position intestinal cGAS as a key driver of obesity through gut-to-fat signalling and suggest that targeting the intestinal cGAS-microbiota IAA axis could offer promising strategies to combat obesity and related metabolic diseases.

Indexed as

Gastrointestinal MicrobiomeIndoleacetic AcidsInterferon Type IMembrane ProteinsNucleotidyltransferasesObesityAnimalscGAS-STING Signaling PathwayCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDown-RegulationHumansIntestinesMaleMiceMice, Inbred C57BLSignal TransductioncGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseIndoleacetic AcidsInterferon Type IMembrane ProteinsNucleotidyltransferasesSting1 protein, mouseSTING Protein

Identifiers

PMID42618739

What OpenQuestion holds

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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.