Evidence map›Paper›PMID 27895397›Full record

ReviewWorld journal of gastroenterology2016

Th17 involvement in nonalcoholic fatty liver disease progression to non-alcoholic steatohepatitis.

Carla Melisa Chackelevicius, Sabrina Eliana Gambaro, Claudio Tiribelli, Natalia Rosso

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  15. Article
  16. The role of REV-ERB in NASH.Acta pharmacologica Sinica · 2022
    Article
  17. Roles for the mycobiome in liver disease.Liver international : official journal of the International Association for the Study of the Liver · 2022
    Review
  18. Digoxin mitigates diethylnitrosamine-induced acute liver injury in mice via limiting production of inflammatory mediators.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Carla Melisa ChackeleviciusCarla Melisa Chackelevicius, Sabrina Eliana Gambaro, Claudio Tiribelli, Natalia Rosso, Italian Liver Foundation, Area Science Park, Trieste, 34149 TS, Italy.
Sabrina Eliana GambaroCarla Melisa Chackelevicius, Sabrina Eliana Gambaro, Claudio Tiribelli, Natalia Rosso, Italian Liver Foundation, Area Science Park, Trieste, 34149 TS, Italy.
Claudio TiribelliCarla Melisa Chackelevicius, Sabrina Eliana Gambaro, Claudio Tiribelli, Natalia Rosso, Italian Liver Foundation, Area Science Park, Trieste, 34149 TS, Italy.
Natalia RossoCarla Melisa Chackelevicius, Sabrina Eliana Gambaro, Claudio Tiribelli, Natalia Rosso, Italian Liver Foundation, Area Science Park, Trieste, 34149 TS, Italy.
Fondazione Italiana Fegato · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. NAFLD encompasses a wide histological spectrum ranging from benign simple steatosis to non-alcoholic steatohepatitis (NASH). Sustained inflammation in the liver is critical in this process. Hepatic macrophages, including liver resident macropaghes (Kupffer cells), monocytes infiltrating the injured liver, as well as specific lymphocytes subsets play a pivotal role in the initiation and perpetuation of the inflammatory response, with a major deleterious impact on the progression of fatty liver to fibrosis. During the last years, Th17 cells have been involved in the development of inflammation not only in liver but also in other organs, such as adipose tissue or lung. Differentiation of a naïve T cell into a Th17 cell leads to pro-inflammatory cytokine and chemokine production with subsequent myeloid cell recruitment to the inflamed tissue. Th17 response can be mitigated by T regulatory cells that secrete anti-inflammatory cytokines. Both T cell subsets need TGF-β for their differentiation and a characteristic plasticity in their phenotype may render them new therapeutic targets. In this review, we discuss the role of the Th17 pathway in NAFLD progression to NASH and to liver fibrosis analyzing different animal models of liver injury and human studies.

Indexed as

AnimalsCell DifferentiationCytokinesDisease Models, AnimalDisease ProgressionHumansInflammation MediatorsLiverLymphocyte ActivationNon-alcoholic Fatty Liver DiseasePhenotypeSignal TransductionTh17 CellsCytokinesInflammation MediatorsInflammationInterleukin-17Nonalcoholic fatty liver diseaseNon-alcoholic steatohepatitisTh17

Identifiers

PMID27895397
PMCPMC5107591
OpenAlexW2548517585

What OpenQuestion holds

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LicenceCC BY-NC
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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.