Clues to quality of journals
Open Access Policy of Helmholtz Association 2016
CC Licencences
Publication Metrics
Home
Deutsch
New EVA Application
Advanced Search
Browse by ...
Publication overview
Statistics (last 5 years)
OA Publications
Submit Publication
Import publication from...
Report missing publication
Contact persons
Help
Text
Endnote (RIS)
BibTeX
Publ. Version/Full Text
DOI
PMC
 |
Open Access Hybrid |
|
as soon as is submitted to ZB.
The complex function of macrophages and their subpopulations in metabolic injury associated fatty liver disease.
J. Physiol.-London 601, 1159-1171 (2023)
Nonalcoholic fatty liver disease (NAFLD), recently re-named to metabolic dysfunction associated fatty liver disease (MAFLD) is a major health problem, as it affects ∼25% of the population globally and is a major cause of hepatic cirrhosis and thereby liver failure, as well as hepatocellular carcinoma (HCC). MALFD comprises a broad range of pathological conditions in the liver, including simple fat accumulation (steatosis) and the more progressive non-alcoholic steatohepatitis (NASH) that can lead to fibrosis development. Cells of innate immunity, and particularly macrophages, comprising the liver resident Kupffer cells and the recruited monocyte-derived macrophages play complex roles in NASH-related inflammation and disease progression to fibrosis. Here, we discuss the recent developments with regards to the function of liver macrophage subpopulations during MAFLD development and progression. Abstract figure legend: Liver macrophages in metabolic dysfunction associated fatty liver disease. Different liver macrophage subpopulations, including Kupffer cells (KC) and monocyte-derived macrophages (MoMf), play multiple roles in the pathogenesis and progression of metabolic dysfunction associated fatty liver disease (MAFLD). This article is protected by copyright. All rights reserved.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Altmetric
5.500
0.000
2
Annotations
Special Publikation
Hide on homepage
Publication type
Article: Journal article
Document type
Review
Keywords
Nash ; Skeynafld ; Inflammation ; Macrophages; Hepatic Stellate Cells; Kupffer Cells; Nonalcoholic Steatohepatitis; Fibrosis; Inflammation; Receptor; Nash; Pathogenesis; Cholesterol; Steatosis
Language
english
Publication Year
2023
HGF-reported in Year
2023
ISSN (print) / ISBN
0022-3751
e-ISSN
1469-7793
Journal
Journal of Physiology - London
Quellenangaben
Volume: 601,
Issue: 7,
Pages: 1159-1171
Publisher
Wiley
Publishing Place
Noboken, UK
Reviewing status
Peer reviewed
Institute(s)
Institute of Pancreatic Islet Research (IPI)
POF-Topic(s)
90000 - German Center for Diabetes Research
Research field(s)
Helmholtz Diabetes Center
PSP Element(s)
G-502600-008
Grants
Deutsche Forschungsgemeinschaft
Sonderzuweisung zur Unterstuetzung profilbestimmender Struktureinheiten 2021' by the SMWK(Saxon State Ministry of Science, Culture and Tourism)
DEEP-HCC project of the LiSyM-cancer program of the BMBF (Federal Ministry of Education and Research)
Sonderzuweisung zur Unterstuetzung profilbestimmender Struktureinheiten 2021' by the SMWK(Saxon State Ministry of Science, Culture and Tourism)
DEEP-HCC project of the LiSyM-cancer program of the BMBF (Federal Ministry of Education and Research)
DOI
10.1113/JP283820
WOS ID
000947855100001
Scopus ID
85150603032
PubMed ID
36825510
Erfassungsdatum
2023-03-01