Evidence map›Paper›PMID 22661952›Full record

ArticleFrontiers in physiology2012

Toll-like receptors in liver fibrosis: cellular crosstalk and mechanisms.

Ling Yang, Ekihiro Seki

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. DAMPs Drive Fibroinflammatory Changes in the Glaucomatous ONH.Investigative ophthalmology & visual science · 2024
    Article
  12. A Paradoxical Tumor Antigen Specific Response in the Liver.bioRxiv : the preprint server for biology · 2024
    Article
  13. Review
  14. Review
  15. Review
  16. The Fibro-Inflammatory Response in the Glaucomatous Optic Nerve Head.International journal of molecular sciences · 2023
    Review
  17. Hybrid Material Based onBiomolecules · 2023
    Article
  18. Alcohol, the gut microbiome, and liver disease.Journal of gastroenterology and hepatology · 2023
    Review
  19. Review
  20. Article

46 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Ling YangDivision of Gastroenterology, Department of Medicine, University of California San Diego, School of Medicine La Jolla, CA, USA.
Ekihiro Seki
University of California, San Diego · US

Funding

LPS binding to TLR4 regulates hepatic stellate cell activation and fibrosisR01DK085252 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI EKIHIRO SEKI · 2011 to 2026
$4.8M
The UCSD Digestive Diseases Research Development CenterR24DK080506 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ECKMANN, LARS · 2008 to 2012
$2.7M
Synergistic Actions By Multiple Toll-Like Receptors in Alcoholic Liver DiseaseR01AA020172 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SEKI, EKIHIRO · 2010 to 2014
$1.8M
NIAAA NIH HHS R01 AA020172NIDDK NIH HHS R01 DK085252NIDDK NIH HHS R24 DK080506
6 · The paper itself

Abstract

Toll-like receptors (TLRs) are pattern recognition receptors that distinguish conserved microbial products, also known as pathogen-associated molecular patterns (PAMPs), from host molecules. Liver is the first filter organ between the gastrointestinal tracts and the rest of the body through portal circulation. Thus, the liver is a major organ that must deal with PAMPs and microorganisms translocated from the intestine and to respond to the damage associated molecular patterns (DAMPs) released from injured organs. These PAMPs and DAMPs preferentially activate TLR signaling on various cell types in the liver inducing the production of inflammatory and fibrogenic cytokines that initiate and prolong liver inflammation, thereby leading to fibrosis. We summarize recent findings on the role of TLRs, ligands, and intracellular signaling in the pathophysiology of liver fibrosis due to different etiology, as well as to highlight the potential role of TLR signaling in liver fibrosis associated with hepatitis C infection, non-alcoholic and alcoholic steatoheoatitis, primary biliary cirrhosis, and cystic fibrosis.

Indexed as

alcoholic liver diseasecystic fibrosishepatitis Cnon-alcoholic steatohepatitisprimary biliary cirrhosistoll-like receptors

Identifiers

PMID22661952
PMCPMC3357552
OpenAlexW1996462805

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.