Hepatocyte mARC1 promotes fatty liver disease.
Hepatic steatosis
Mendelian randomisation
NASH
Triglycerides
Journal
JHEP reports : innovation in hepatology
ISSN: 2589-5559
Titre abrégé: JHEP Rep
Pays: Netherlands
ID NLM: 101761237
Informations de publication
Date de publication:
May 2023
May 2023
Historique:
received:
02
09
2022
revised:
19
01
2023
accepted:
21
01
2023
medline:
1
5
2023
pubmed:
1
5
2023
entrez:
1
5
2023
Statut:
epublish
Résumé
Non-alcoholic fatty liver disease (NAFLD) has a prevalence of ∼25% worldwide, with significant public health consequences yet few effective treatments. Human genetics can help elucidate novel biology and identify targets for new therapeutics. Genetic variants in mitochondrial amidoxime-reducing component 1 ( Analyses including multi-trait colocalisation and Mendelian randomisation were used to assess the genetic associations of We showed that genetic variants within the Collectively, our findings from human genetics, and We report that genetically predicted increases in
Sections du résumé
Background & Aims
UNASSIGNED
Non-alcoholic fatty liver disease (NAFLD) has a prevalence of ∼25% worldwide, with significant public health consequences yet few effective treatments. Human genetics can help elucidate novel biology and identify targets for new therapeutics. Genetic variants in mitochondrial amidoxime-reducing component 1 (
Methods
UNASSIGNED
Analyses including multi-trait colocalisation and Mendelian randomisation were used to assess the genetic associations of
Results
UNASSIGNED
We showed that genetic variants within the
Conclusions
UNASSIGNED
Collectively, our findings from human genetics, and
Impact and implications
UNASSIGNED
We report that genetically predicted increases in
Identifiants
pubmed: 37122688
doi: 10.1016/j.jhepr.2023.100693
pii: S2589-5559(23)00024-1
pmc: PMC10133763
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100693Informations de copyright
© 2023 The Author(s).
Déclaration de conflit d'intérêts
A provisional patent application directed to the subject matter disclosed in this manuscript has been filed by Novo Nordisk A/S. LCL, LC, LSH, RRK, CM, JN, CED, STH, RP, IS, EJL, TND, AC, SH, BG, MEG, ETM, AHAE, WGH, KC, JF, JMMH, BA, and MAR are Novo Nordisk A/S or Novo Nordisk Ltd employees. EW and NWP are former Dicerna employees. SBR is a former employee of Dicerna Pharmaceuticals Inc. and presently employed by the Novartis Institutes for BioMedical Research (NIBR), Cambridge, MA, USA. WL is a former employee of Dicerna Pharmaceuticals and presently employed with Biogen Inc, Cambridge, MA, USA. LH is a scientific consultant for Novo Nordisk A/S. The remaining authors declare no competing interests. Please refer to the accompanying ICMJE disclosure forms for further details.
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