Evidence map›Paper›PMID 42410595›Full record

ArticleCell communication and signaling : CCS2026

Specific bile acids can elicit the type-I interferon response through the cGAS-STING pathway.

Jianan He, Ziyan Huang, Caiwan Xiong, Zhicheng Huang, Hao Yan, Bing Sun, Xing Liu, Yong Cao, Xun Chen, Huabin Li and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2026. 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. Review
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.

Jianan HeNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Ziyan HuangNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Caiwan XiongNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Zhicheng HuangNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Hao YanNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Bing SunState Key Laboratory of Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Xing LiuNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Yong CaoNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Xun ChenNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Huabin LiDepartment of Otolaryngology, Eye & ENT Hospital, Fudan University, Shanghai, 200031, China. allergyli@163.com.
Limin CaoNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China. lmcao@simm.ac.cn.
Hui XiaoNational Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China. huixiao@simm.ac.cn.

Funding

the National Key Research and Development Program of China 2021YFA1301400the National Natural Science Foundation of China grant 32030040the Strategic Priority Research Program of the Chinese Academy of Sciences XDB0940102
6 · The paper itself

Abstract

Bile acids are metabolites crucial to lipid metabolism and immune regulation, yet their biological functions and mechanistic underpinnings remain largely elusive. In this study, we demonstrate that specific bile acids DCA, CDCA and LCA can trigger the type-I interferon response (IFN-I) in various cells through the cytosolic DNA-sensing cGAS-STING pathway. Phosphoproteomics indicates that bile acids can elicit a wide array of changes across numerous signaling pathways, culminating in the downregulation of Bcl-2 and p-BAD, resulting in the formation of Bax/Bak pore for the cytosolic release of mitochondrial DNA. The induction of the IFN-I response also depends on inter-organelle interactions among the endolysosome, ER, and mitochondria, leading to calcium flux and mitochondrial dysfunction, which also contribute to mtDNA release. Further, while systemic administration of bile acid DCA can trigger the STING-dependent IFN-I response in various tissues and bloodstream, tissue-restricted application of DCA can exert antiviral and antitumor effects. Together, these findings identify the cGAS-STING pathway as a mechanistic underpinning of specific bile acids and provide new insights into harnessing bile acids for future therapy.

Indexed as

Bile Acids and SaltsInterferon Type IMembrane ProteinsNucleotidyltransferasesAnimalscGAS-STING Signaling PathwayCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, MitochondrialHumansMitochondriaSignal TransductionSTING ProteinBile Acids and SaltscGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, MitochondrialInterferon Type IMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinBile acidCalcium fluxcGASInfluenza virusMitochondria fissionSTINGType-I interferon

Identifiers

PMID42410595
PMCPMC13625343

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.