Evidence map›Paper›PMID 37240132›Full record

ArticleInternational journal of molecular sciences2023

PEMT Mediates Hepatitis C Virus-Induced Steatosis, Explains Genotype-Specific Phenotypes and Supports Virus Replication.

Mosleh Abomughaid, Enoch S E Tay, Russell Pickford, Chandra Malladi, Scott A Read, Jens R Coorssen, Brian S Gloss, Jacob George, Mark W Douglas

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Mosleh AbomughaidStorr Liver Centre, The Westmead Institute for Medical Research, The University of Sydney and Westmead Hospital, Sydney, NSW 2145, Australia.ORCID 0000-0001-9663-8874
Enoch S E TayStorr Liver Centre, The Westmead Institute for Medical Research, The University of Sydney and Westmead Hospital, Sydney, NSW 2145, Australia.
Russell PickfordBioanalytical Mass Spectrometry Facility, Mark Wainright Analytical Centre, University of New South Wales, Sydney, NSW 2052, Australia.
Chandra MalladiDepartment of Molecular Physiology, School of Medicine, Western Sydney University, Sydney, NSW 2751, Australia.
Scott A ReadStorr Liver Centre, The Westmead Institute for Medical Research, The University of Sydney and Westmead Hospital, Sydney, NSW 2145, Australia.ORCID 0000-0001-6775-2061
Jens R CoorssenDepartment of Molecular Physiology, School of Medicine, Western Sydney University, Sydney, NSW 2751, Australia.ORCID 0000-0001-8048-7370
Brian S GlossWestmead Research Hub, Westmead Institute for Medical Research, Sydney, NSW 2145, Australia.
Jacob GeorgeStorr Liver Centre, The Westmead Institute for Medical Research, The University of Sydney and Westmead Hospital, Sydney, NSW 2145, Australia.ORCID 0000-0002-8421-5476
Mark W DouglasStorr Liver Centre, The Westmead Institute for Medical Research, The University of Sydney and Westmead Hospital, Sydney, NSW 2145, Australia.ORCID 0000-0003-4621-3485
The University of Sydney · AUBrock University · CAWestern Sydney University · AUWestmead Institute for Medical Research · AU

Funding

Ministry of Health PhD Overseas ScholarshipNational Health and Medical Research Council 1003767National Health and Medical Research Council 1047417National Health and Medical Research Council 1053206University of Sydney Robert W Storr bequest to the Sydney Medical FoundationUniversity of Sydney University of Sydney DVC Research/Postdoctoral Research Fellowship Scheme
6 · The paper itself

Abstract

The hepatitis C virus (HCV) relies on cellular lipid pathways for virus replication and also induces liver steatosis, but the mechanisms involved are not clear. We performed a quantitative lipidomics analysis of virus-infected cells by combining high-performance thin-layer chromatography (HPTLC) and mass spectrometry, using an established HCV cell culture model and subcellular fractionation. Neutral lipid and phospholipids were increased in the HCV-infected cells; in the endoplasmic reticulum there was an ~four-fold increase in free cholesterol and an ~three-fold increase in phosphatidyl choline (

Indexed as

Fatty LiverHepatitis CHepatitis C, ChronicCholesterolGenotypeHepacivirusHumansPhenotypePhosphatidylcholinesPhosphatidylethanolamine N-MethyltransferaseTransferasesVirus ReplicationCholesterolPEMT protein, humanPhosphatidylcholinesPhosphatidylethanolamine N-MethyltransferaseTransferaseshepatitis C viruslipid metabolismlipidomicsPEMTphosphatidyl cholinesteatosis

Identifiers

PMID37240132
PMCPMC10218061
OpenAlexW4376890824

What Socratic 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 Socratic graph.