Evidence map›Paper›PMID 33298885›Full record

ArticleCell death & disease2020

Hepatocyte cannabinoid 1 receptor nullification alleviates toxin-induced liver damage via NF-κB signaling.

Yoo Kim, Sudeep Gautam, Kanikkai Raja Aseer, Jaekwan Kim, Prabha Chandrasekaran, Caio Henrique Mazucanti, Paritosh Ghosh, Jennifer F O'Connell, Máire E Doyle, Ashley Appleton and 3 more

Abstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–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

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. The Role of Cannabidiol in Liver Disease: A Systemic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Antioxidant Effects ofFrontiers in pharmacology · 2021
    Article
  14. 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

13 authors.

Yoo KimLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0002-4525-1319
Sudeep GautamLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Kanikkai Raja AseerLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Jaekwan KimLaboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Prabha ChandrasekaranLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Caio Henrique MazucantiLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Paritosh GhoshLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Jennifer F O'ConnellLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Máire E DoyleLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Ashley AppletonLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Elin LehrmannLaboratory of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Qing-Rong LiuLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0001-8477-6452
Josephine M EganLaboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. eganj@grc.nia.nih.gov.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cannabinoid 1 receptor (CB1R) expression is upregulated in the liver with viral hepatitis, cirrhosis, and both alcoholic and non-alcoholic fatty liver disease (FLD), whereas its expression is muted under usual physiological conditions. Inhibiting CB1R has been shown to be beneficial in preserving hepatic function in FLD but it is unclear if inhibiting CB1R during an inflammatory response to an acute hepatic injury, such as toxin-induced injury, would also be beneficial. We found that intrinsic CB1R in hepatocytes regulated liver inflammation-related gene transcription. We tested if nullification of hepatocyte-specific CB1R (hCNR1

Indexed as

Signal TransductionAnimalsApoptosisCell MembraneConcanavalin ACyclic AMPHepatocytesInflammationLiverMaleMiceModels, BiologicalNF-kappa BProtein BindingReceptor, Cannabinoid, CB1Tumor Necrosis Factor-alphaConcanavalin ACyclic AMPNF-kappa BReceptor, Cannabinoid, CB1Tumor Necrosis Factor-alpha

Identifiers

PMID33298885
PMCPMC7726564

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.