Evidence map›Paper›PMID 34027340›Full record

ReviewJHEP reports : innovation in hepatology2021

Genetic predisposition similarities between NASH and ASH: Identification of new therapeutic targets.

Cristiana Bianco, Elia Casirati, Francesco Malvestiti, Luca Valenti

Open access · goldAbstract readReview
In one paragraph

Review in JHEP reports : innovation in hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
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  6. Genetics of Metabolic Dysfunction-associated Steatotic Liver Disease: The State of the Art Update.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2024
    Review
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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

4 authors at 2 institutions in 1 country.

Cristiana BiancoPrecision Medicine - Department of Transfusion Medicine and Hematology, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
Elia CasiratiDepartment of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy.
Francesco MalvestitiDepartment of Pathophysiology and Transplantation, Università degli Studi di Milano, Milan, Italy.
Luca ValentiPrecision Medicine - Department of Transfusion Medicine and Hematology, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy.
University of Milan · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fatty liver disease can be triggered by a combination of excess alcohol, dysmetabolism and other environmental cues, which can lead to steatohepatitis and can evolve to acute/chronic liver failure and hepatocellular carcinoma, especially in the presence of shared inherited determinants. The recent identification of the genetic causes of steatohepatitis is revealing new avenues for more effective risk stratification. Discovery of the mechanisms underpinning the detrimental effect of causal mutations has led to some breakthroughs in the comprehension of the pathophysiology of steatohepatitis. Thanks to this approach, hepatocellular fat accumulation, altered lipid droplet remodelling and lipotoxicity have now taken centre stage, while the role of adiposity and gut-liver axis alterations have been independently validated. This process could ignite a virtuous research cycle that, starting from human genomics, through omics approaches, molecular genetics and disease models, may lead to the development of new therapeutics targeted to patients at higher risk. Herein, we also review how this knowledge has been applied to: a) the study of the main

Indexed as

AA, arachidonic acidalcoholic liver diseaseASH, alcoholic steatohepatitiscirrhosisDAG, diacylglycerolDNL, de novo lipogenesisER, endoplasmic reticulumfatty liver diseaseFFAs, free fatty acidsFGF19, fibroblast growth factor 19FLD, fatty liver diseaseFXR, farnesoid X receptorGCKR, glucokinase regulatorgeneticsGPR55, G protein-coupled receptor 55HCC, hepatocellular carcinomaHFE, homeostatic iron regulatorHSC, hepatic stellate cellsHSD17B13, hydroxysteroid 17-beta dehydrogenase 13IL32IL-, interleukin-interleukin-32LDs, lipid dropletsLPI, lysophosphatidyl-inositolMARC1, mitochondrial amidoxime reducing component 1MBOAT7MBOAT7, membrane bound O-acyltransferase domain-containing 7NASH, non-alcoholic steatohepatitisnon-alcoholic fatty liver diseasePNPLA3PNPLA3, patatin like phospholipase domain containing 3PPAR, peroxisome proliferator-activated receptorprecision medicinePRS, polygenic risk scorePUFAs, polyunsaturated fatty acidsSREBP, sterol response element binding proteinsteatohepatitisTAG, triacylglyceroltherapyTNF-α, tumour necrosis factor-α

Identifiers

PMID34027340
PMCPMC8122117
OpenAlexW3148943158

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.