Evidence map›Paper›PMID 38397122›Full record

ArticleInternational journal of molecular sciences2024

Genetic Ablation of STE20-Type Kinase MST4 Does Not Alleviate Diet-Induced MASLD Susceptibility in Mice.

Mara Caputo, Emma Andersson, Ying Xia, Wei Hou, Emmelie Cansby, Max Erikson, Dan Emil Lind, Bengt Hallberg, Manoj Amrutkar, Margit Mahlapuu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.1field-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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. 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

10 authors at 2 institutions in 2 countries.

Mara CaputoDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Emma AnderssonDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Ying XiaDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Wei HouDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Emmelie CansbyDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Max EriksonDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Dan Emil LindDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Bengt HallbergDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.ORCID 0000-0003-2032-2616
Manoj AmrutkarDepartment of Pathology, Oslo University Hospital Rikshospitalet, 0372 Oslo, Norway.ORCID 0000-0002-1868-0249
Margit MahlapuuDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Sahlgrenska University Hospital · SEOslo University Hospital · NO

Funding

Adlerbertska Foundations N/ADiabetesfonden N/AFamiljen Erling-Perssons Stiftelse N/AI. Hultman Foundation N/AKnut and Alice Wallenberg Foundation N/AMagnus Bergvalls Stiftelse N/ANovo Nordisk Foundation N/AO. E. och Edla Johanssons Vetenskapliga Stiftelse N/ARoyal Society of Arts and Sciences in Gothenburg N/AStiftelsen Sigurd and Elsa Goljes Minne N/ASwedish Cancer Society N/ASwedish Heart-Lung Foundation N/ASwedish Research Council N/AWilhelm & Martina Lundgrens Stiftelser N/A
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) and its advanced subtype, metabolic dysfunction-associated steatohepatitis (MASH), have emerged as the most common chronic liver disease worldwide, yet there is no targeted pharmacotherapy presently available. This study aimed to investigate the possible in vivo function of STE20-type protein kinase MST4, which was earlier implicated in the regulation of hepatocellular lipotoxic milieu in vitro, in the control of the diet-induced impairment of systemic glucose and insulin homeostasis as well as MASLD susceptibility. Whole-body and liver-specific

Indexed as

Fatty LiverMetabolic DiseasesNon-alcoholic Fatty Liver DiseaseAnimalsCholineDiet, High-FatGlucoseHepatocytesHumansInsulinLiverMiceMice, Inbred C57BLMice, KnockoutMice, ObeseCholineGlucoseInsulinintrahepatocellular lipid dropletsliver lipid metabolismmetabolic dysfunction-associated steatohepatitismetabolic dysfunction-associated steatotic liver diseaseMST4

Identifiers

PMID38397122
PMCPMC10888586
OpenAlexW4391926077

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.