Platelets in Non-alcoholic Fatty Liver Disease.
Kupffer cells
antiplatelet agents
fibrosis
hepatic stellate cells
inflammation
non-alcoholic fatty liver disease
non-alcoholic steatohepatitis
platelets
Journal
Frontiers in pharmacology
ISSN: 1663-9812
Titre abrégé: Front Pharmacol
Pays: Switzerland
ID NLM: 101548923
Informations de publication
Date de publication:
2022
2022
Historique:
received:
23
12
2021
accepted:
03
02
2022
entrez:
7
3
2022
pubmed:
8
3
2022
medline:
8
3
2022
Statut:
epublish
Résumé
Non alcoholic steatohepatitis (NASH) is the inflammatory reaction of the liver to excessive accumulation of lipids in the hepatocytes. NASH can progress to cirrhosis and hepatocellular carcinoma (HCC). Fatty liver is the hepatic manifestation of metabolic syndrome. A subclinical inflammatory state is present in patients with metabolic alterations like insulin resistance, type-2 diabetes, obesity, hyperlipidemia, and hypertension. Platelets participate in immune cells recruitment and cytokines-induced liver damage. It is hypothesized that lipid toxicity cause accumulation of platelets in the liver, platelet adhesion and activation, which primes the immunoinflammatory reaction and activation of stellate cells. Recent data suggest that antiplatelet drugs may interrupt this cascade and prevent/improve NASH. They may also improve some metabolic alterations. The pathophysiology of inflammatory liver disease and the implication of platelets are discussed in details.
Identifiants
pubmed: 35250588
doi: 10.3389/fphar.2022.842636
pii: 842636
pmc: PMC8895200
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
842636Informations de copyright
Copyright © 2022 Dalbeni, Castelli, Zoncapè, Minuz and Sacerdoti.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling editor declared a past co-authorship with one of the authors PM.
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