Evidence map›Paper›PMID 42813208›Full record

ReviewLife medicine2026

Bile acids as a "new hormone" in aging-related liver disease.

Buyu Deng, Xingjian Li, Yue Li, Longchuan Han, Zhihui Zou, Yingting Zhang, Jing Luo, Xinxin Tang, Hui Kong, Chenxi Shi and 4 more

Abstract readReview
In one paragraph

Review in Life medicine, 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

14 authors.

Buyu DengInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Xingjian LiInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yue LiInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Longchuan HanInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Zhihui ZouInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yingting ZhangInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Jing LuoInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Xinxin TangInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Hui KongSchool of Exercise and Health, Shanghai University of Sport, Shanghai 200438, China.
Chenxi ShiInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Ying HuangInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.ORCID https://orcid.org/0000-0002-9537-9345
Hanzhi LuoCancer Epigenetics Institute, Fox Chase Cancer Center, Philadelphia, PA 19111, United States.
Yinkun FuInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Ming HeInstitute for Translational Medicine on Cell Fate and Disease, Shanghai Ninth People's Hospital, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bile acids (BAs) have evolved from their classical definition as digestive surfactants to be recognized as potent endocrine signaling molecules that orchestrate systemic metabolism. Through activation of nuclear receptors, such as farnesoid X receptor (FXR), and membrane receptors, such as G protein-coupled BA receptor 1 (GPBAR1/TGR5), BAs regulate glucose, lipid, immune, and energy homeostasis. Aging reshapes BA synthesis, enterohepatic circulation, hydrophobicity, microbial biotransformation, and receptor responsiveness, thereby linking BA metabolism to hepatic senescence, inflammaging, and age-associated liver vulnerability. In turn, dysregulated BA signaling can amplify mitochondrial stress, endoplasmic reticulum stress, impaired autophagy, immune dysfunction, and senescence-associated secretory phenotypes, suggesting a bidirectional relationship between BA remodeling and aging progression. This review critically examines the role of BAs as hormone-like mediators within the aging liver microenvironment, summarizes major BA species and receptor preferences, integrates gut microbiota-BA crosstalk, and evaluates the therapeutic potential and caveats of targeting the BA-FXR-TGR5 axis in aging-related liver diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD), alcohol-associated liver disease (ALD), autoimmune liver diseases (AILD), chronic hepatitis B (CHB), and hepatocellular carcinoma (HCC).

Indexed as

agingbile acidsfarnesoid X receptorG protein-coupled bile acid receptor 1hormone-like signaling

Identifiers

PMID42813208
PMCPMC13623503

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.