Evidence map›Paper›PMID 29456458›Full record

ArticleProteome science2018

Proteomic identification and characterization of hepatic glyoxalase 1 dysregulation in non-alcoholic fatty liver disease.

Christos Spanos, Elaina M Maldonado, Ciarán P Fisher, Petchpailin Leenutaphong, Ernesto Oviedo-Orta, David Windridge, Francisco J Salguero, Alexandra Bermúdez-Fajardo, Mark E Weeks, Caroline Evans and 10 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Proteome science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 8 institutions in 3 countries.

Christos Spanos1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.
Elaina M Maldonado1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.
Ciarán P Fisher1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.
Petchpailin Leenutaphong1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.
Ernesto Oviedo-Orta1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.
David Windridge1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.
Francisco J Salguero1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.
Alexandra Bermúdez-Fajardo1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.
Mark E Weeks2Institute of Child Health, University College London, WC1N 1EH, London, UK.
Caroline Evans3Biological and Systems Engineering Group, ChELSI Institute, Department of Chemical and Biological Engineering, University of Sheffield, S1 3JD, Sheffield, UK.
Bernard M Corfe4Molecular Gastroenterology Research Group, Department of Oncology and Insigneo Institute for in silico Medicine, University of Sheffield, S10 2RX, Sheffield, UK.
Naila RabbaniClinical Sciences Research Laboratories, Warwick Medical School, University of Warwick, University Hospital, Coventry, CV2 2DX UK.
Paul J ThornalleyClinical Sciences Research Laboratories, Warwick Medical School, University of Warwick, University Hospital, Coventry, CV2 2DX UK.
Michael H Miller6Medical Research Institute, University of Dundee, Ninewells Hospital and Medical School, Dundee, DD1 9SY UK.
Huan Wang6Medical Research Institute, University of Dundee, Ninewells Hospital and Medical School, Dundee, DD1 9SY UK.
John F Dillon6Medical Research Institute, University of Dundee, Ninewells Hospital and Medical School, Dundee, DD1 9SY UK.
Alberto Quaglia7Paediatric Liver, GI and Nutrition Centre, King's College London School of Medicine, London, SE5 9RS UK.
Anil Dhawan7Paediatric Liver, GI and Nutrition Centre, King's College London School of Medicine, London, SE5 9RS UK.
Emer Fitzpatrick7Paediatric Liver, GI and Nutrition Centre, King's College London School of Medicine, London, SE5 9RS UK.
J Bernadette Moore1Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, GU2 7XH UK.ORCID 0000-0003-4750-1550
University of Surrey · GBKing's College London · GBUniversity of Dundee · GBUniversity Hospital Coventry · GBInsigneo · GBInstitute of Child Health · INUniversity of Leeds · GBUniversity of Sheffield · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. However, its molecular pathogenesis is incompletely characterized and clinical biomarkers remain scarce. The aims of these experiments were to identify and characterize liver protein alterations in an animal model of early, diet-related, liver injury and to assess novel candidate biomarkers in NAFLD patients. Methods: Liver membrane and cytosolic protein fractions from high fat fed apolipoprotein E knockout (ApoE Results: Through proteomic profiling, we identified decreased expression of hepatic glyoxalase 1 (GLO1) in a murine model. GLO1 protein expression was also found altered in tissue biopsies from paediatric NAFLD patients. In vitro experiments demonstrated that, in response to lipid loading in hepatocytes, GLO1 is first hyperacetylated then ubiquitinated and degraded, leading to an increase in reactive methylglyoxal. In a cohort of 59 biopsy-confirmed adult NAFLD patients, increased serum levels of the primary methylglyoxal-derived advanced glycation endproduct, hydroimidazolone (MG-H1) were significantly correlated with body mass index ( Conclusion: Collectively these results demonstrate the dysregulation of GLO1 in NAFLD and implicate the acetylation-ubquitination degradation pathway as the functional mechanism. Further investigation of the role of GLO1 in the molecular pathogenesis of NAFLD is warranted.

Indexed as

GlyoxalaseiTRAQMethylglyoxalNon-alcoholic fatty liver diseaseProteomics

Identifiers

PMID29456458
PMCPMC5813374
OpenAlexW2791251135

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.