Alcohol-Associated Liver Disease Outcomes: Critical Mechanisms of Liver Injury Progression.
MetAld
alcohol-associated liver disease
cell death
epigenetics
fatty acid binding protein 4
fibrosis
hemolysis
hepatic stellate cells
hepatocellular carcinoma
models
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
27 Mar 2024
27 Mar 2024
Historique:
received:
22
02
2024
revised:
20
03
2024
accepted:
24
03
2024
medline:
27
4
2024
pubmed:
27
4
2024
entrez:
27
4
2024
Statut:
epublish
Résumé
Alcohol-associated liver disease (ALD) is a substantial cause of morbidity and mortality worldwide and represents a spectrum of liver injury beginning with hepatic steatosis (fatty liver) progressing to inflammation and culminating in cirrhosis. Multiple factors contribute to ALD progression and disease severity. Here, we overview several crucial mechanisms related to ALD end-stage outcome development, such as epigenetic changes, cell death, hemolysis, hepatic stellate cells activation, and hepatic fatty acid binding protein 4. Additionally, in this review, we also present two clinically relevant models using human precision-cut liver slices and hepatic organoids to examine ALD pathogenesis and progression.
Identifiants
pubmed: 38672422
pii: biom14040404
doi: 10.3390/biom14040404
pii:
doi:
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM