Evidence map›Paper›PMID 34064187›Full record

ReviewCells2021

Bile Acids Activated Receptors in Inflammatory Bowel Disease.

Michele Biagioli, Silvia Marchianò, Adriana Carino, Cristina Di Giorgio, Luca Santucci, Eleonora Distrutti, Stefano Fiorucci

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 88 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Bile acid signaling in health and disease.Molecular biomedicine · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. The Herbal PairFood science & nutrition · 2025
    Article
  18. Review
  19. Article
  20. Regulation of innate lymphoid cell by microbial metabolites.Journal of molecular medicine (Berlin, Germany) · 2025
    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

7 authors at 2 institutions in 1 country.

Michele BiagioliDepartment of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy.ORCID 0000-0002-2995-6896
Silvia MarchianòDepartment of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy.
Adriana CarinoDepartment of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy.ORCID 0000-0003-2341-9528
Cristina Di GiorgioDepartment of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy.
Luca SantucciAzienda Ospedaliera di Perugia, 06132 Perugia, Italy.
Eleonora DistruttiAzienda Ospedaliera di Perugia, 06132 Perugia, Italy.
Stefano FiorucciDepartment of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy.ORCID 0000-0003-3816-4222
University of Perugia · ITAzienda Ospedaliera di Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Once known exclusively for their role in nutrients absorption, bile acids have emerged as signaling molecules, generated from cholesterol breakdown, acting on several immune cells by activating a variety of receptors including the G protein-coupled bile acid receptor 1 (GPABR1 or TGR5), the Farnesoid-X-receptor (FXR) and, as recently discovered, the retinoid-related orphan receptors (ROR)γt. GPBAR1, FXR, and RORγt are highly expressed in cells of the innate and adaptive immune system (i.e., dendritic cells (DCs), macrophages, innate lymphoid 3 cells (ILC3s), and T helper 17 (Th17) lymphocytes) and plays an important role in regulating intestinal and liver immunity, highlighting a role for various bile acid species in regulating immune responses to intestinal microbial antigens. While primary bile acids are generated from the cholesterol breakdown secondary bile acids, the GPBAR1 ligands, and oxo-bile acids derivatives, the RORγt ligands, are generated by the intestinal microbiota, highlighting the potential of these bile acids in mediating the chemical communication between the intestinal microbiota and the host. Changes in intestinal microbiota, dysbiosis, alter the composition of the bile acid pool, promoting the activation of the immune system and development of chronic inflammation. In this review, we focus on the molecular mechanisms by which an altered bile acid signaling promotes intestinal inflammation.

Indexed as

Bile Acids and SaltsImmunity, InnateInflammatory Bowel DiseasesAnimalsGastrointestinal MicrobiomeHumansReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptors, G-Protein-CoupledBile Acids and SaltsGPBAR1 protein, humanReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearReceptors, G-Protein-Coupledbile acidsFXRGPBAR1intestinal immunityintestinal microiotaRORγt

Identifiers

PMID34064187
PMCPMC8224328
OpenAlexW3162040744

What OpenQuestion 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 OpenQuestion graph.