Evidence map›Paper›PMID 29449533›Full record

ArticleCell death & disease2018

Non-alcoholic fatty liver disease severity is modulated by transglutaminase type 2.

Mauro Piacentini, Andrea Baiocchini, Franca Del Nonno, Gerry Melino, Nickolai A Barlev, Federica Rossin, Manuela D'Eletto, Laura Falasca

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Protective role of arnebin-1 in rats with nonalcoholic fatty liver disease.The Journal of international medical research · 2019
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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

8 authors at 4 institutions in 2 countries.

Mauro PiacentiniNational Institute for Infectious Diseases, IRCCS "Lazzaro Spallanzani", Rome, Italy. mauro.piacentini@uniroma2.it.
Andrea BaiocchiniNational Institute for Infectious Diseases, IRCCS "Lazzaro Spallanzani", Rome, Italy.
Franca Del NonnoNational Institute for Infectious Diseases, IRCCS "Lazzaro Spallanzani", Rome, Italy.
Gerry MelinoDepartment Experimental Medicine and Surgery, University of Rome "Tor Vergata", Rome, Italy.
Nickolai A BarlevInstitute of Cytology Russian Academy of Sciences, Saint-Petersburg, Russian Federation.
Federica RossinDepartment of Biology, University of Rome "Tor Vergata", Rome, Italy.
Manuela D'ElettoDepartment of Biology, University of Rome "Tor Vergata", Rome, Italy.
Laura FalascaNational Institute for Infectious Diseases, IRCCS "Lazzaro Spallanzani", Rome, Italy. laura.falasca@inmi.it.
Istituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · ITUniversity of Rome Tor Vergata · ITInstitute of Cytology · RUIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

Medical Research Council MC_U132670600
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is one of the most important liver diseases worldwide. Currently, no effective treatment is available, and NAFLD pathogenesis is incompletely understood. Transglutaminase type 2 (TG2) is a ubiquitous enzyme whose dysregulation is implicated in the pathogenesis of various human diseases. Here we examined the impact of TG2 on NAFLD progression using the high-fat-diet-induced model in both wild-type and TG2-deficient mice. Animals were fed with a standard chow diet or a high-fat diet (42% of the energy from fat) for 16 weeks. Results demonstrated that the absence of a functional enzyme, which causes the impairment of autophagy/mitophagy, leads to worsening of disease progression. Data were confirmed by pharmacological inhibition of TG2 in WT animals. In addition, the analysis of human liver samples from NAFLD patients validated the enzyme's involvement in the liver fat disease pathogenesis. Our findings strongly suggest that TG2 activation may offer protection in the context of NAFLD, thus representing a novel therapeutic target for tackling the NAFLD progression.

Indexed as

AnimalsAutophagy-Related ProteinsDiet, High-FatDisease Models, AnimalEnzyme InhibitorsGTP-Binding ProteinsHumansLiverMaleMice, Inbred C57BLMice, KnockoutMitochondria, LiverMitophagyNon-alcoholic Fatty Liver DiseaseProtein Glutamine gamma Glutamyltransferase 2Signal TransductionAutophagy-Related ProteinsEnzyme InhibitorsGTP-Binding ProteinsProtein Glutamine gamma Glutamyltransferase 2Transglutaminases

Identifiers

PMID29449533
PMCPMC5833377
OpenAlexW2791846703

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.