PuSH - Publication Server of Helmholtz Zentrum München

Subramanian, P.* ; Hampe, J.* ; Tacke, F.* ; Chavakis, T.

Fibrogenic pathways in metabolic dysfunction associated fatty liver disease (MAFLD).

Int. J. Mol. Sci. 23:6996 (2022)
Publ. Version/Full Text DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re-defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting ~25% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non-alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH-related fibrosis. Here, we discuss the profibrogenic pathways, which lead to HSC activation and fibrogenesis, with a particular focus on the intercellular hepatocyte-HSC and macrophage-HSC crosstalk.
Impact Factor
Scopus SNIP
Altmetric
6.208
0.000
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Review
Keywords Fibrosis ; Hepatic Stellate Cells ; Hepatocyte ; Macrophage ; Metabolic Associated Fatty Liver Disease ; Nonalcoholic Fatty Liver Disease ; Nonalcoholic Steatohepatitis
Language english
Publication Year 2022
HGF-reported in Year 2022
ISSN (print) / ISBN 1661-6596
e-ISSN 1422-0067
Quellenangaben Volume: 23, Issue: 13, Pages: , Article Number: 6996 Supplement: ,
Publisher MDPI
Publishing Place Basel
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 Federal Ministry of Education and Research
PubMed ID 35805998
Erfassungsdatum 2022-10-27