Evidence map›Paper›PMID 30483776›Full record

ReviewMolecular medicine reports2019

Roles of the inflammasome in the gut‑liver axis (Review).

Junfeng Wang, Rui Dong, Shan Zheng

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Inflammation: A New Look at an Old Problem.International journal of molecular sciences · 2022
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Bile Acid Toxicity and Protein Kinases.Advances in experimental medicine and biology · 2021
    Article
  18. Article
  19. Pattern Recognition Receptors: Significance of Expression in the Liver.Archivum immunologiae et therapiae experimentalis · 2020
    Review
  20. Article
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

3 authors at 1 institution in 1 country.

Junfeng WangDepartment of Pediatric Surgery, Children's Hospital of Fudan University, Shanghai Key Laboratory of Birth Defect, Shanghai 201102, P.R. China.
Rui DongDepartment of Pediatric Surgery, Children's Hospital of Fudan University, Shanghai Key Laboratory of Birth Defect, Shanghai 201102, P.R. China.
Shan ZhengDepartment of Pediatric Surgery, Children's Hospital of Fudan University, Shanghai Key Laboratory of Birth Defect, Shanghai 201102, P.R. China.
Children's Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gut‑liver axis connects the liver with the intestine via bile acid metabolism. Bile acid dysregulation leads to intestinal dysbiosis, that allows enterogenous pathogenic bacteria, including Gram‑negative bacteria and their products lipopolysaccharide (LPS), into the liver via the portal vein, triggering inflammation in the liver. The inflammasome serves as an intracellular pattern recognition receptor that detects pathogens or danger signals and mediates innate immunity in the liver or gut. Specifically, the NACHT, LRR and PYD domains‑containing protein (NLRP)6 inflammasome maintains intestinal microbial balance, by promoting interleukin (IL)‑18‑dependent antimicrobial peptide synthesis and mucus secretion from goblet cells. The NLRP3 inflammasome, in contrast, primarily induces IL‑1β and aggravates inflammatory liver injury. Furthermore, the NLRP3 inflammasome affects the epithelial integrity of cholangiocytes by inducing the production of pro‑inflammatory cytokines. In addition, bile acids, including deoxycholic acid and chenodeoxycholic acid, are able to activate the NLRP3 inflammasome in macrophages; however, bile acids have the potential to exert the opposite role by interacting with the membrane‑bound Takeda G‑protein receptor 5 or by activating nuclear farnesoid‑X receptor. Therefore, further investigation of the molecular mechanisms underlying the inflammasome, involved in the gut‑liver axis, may provide important insights into the identification of a potential therapeutic target for the treatment of liver and gut diseases. The present review discusses the roles of the inflammasome in the gut‑liver axis, and the emerging associations between the inflammasome and the intestinal microbiota or the bile acids in the gut‑liver axis.

Indexed as

AnimalsBile Acids and SaltsHumansInflammasomesIntestinal MucosaIntestinesLiverMacrophagesSignal TransductionBile Acids and SaltsInflammasomesbile acidgut-liver axisinflammationintestinal microbiotaNLRP3 inflammasomeNLRP6 inflammasome

Identifiers

PMID30483776
PMCPMC6297761
OpenAlexW2900541582

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.