Titre
Gap junctions in liver disease: Implications for pathogenesis and therapy.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Hernández-Guerra, M.
Auteure/Auteur
Hadjihambi, A.
Auteure/Auteur
Jalan, R.
Auteure/Auteur
Liens vers les unités
ISSN
1600-0641
Statut éditorial
Publié
Date de publication
2019-04
Volume
70
Numéro
4
Première page
759
Dernière page/numéro d’article
772
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Review
Publication Status: ppublish
Publication Status: ppublish
Résumé
In the normal liver, cells interact closely through gap junctions. By providing a pathway for the trafficking of low molecular mass molecules, these channels contribute to tissue homeostasis and maintenance of hepatic function. Thus, dysfunction of gap junctions affects a wide variety of liver processes, such as differentiation, cell death, inflammation and fibrosis. In fact, dysfunctional gap junctions have been implicated, for more than a decade, in cholestatic disease, hepatic cancer and cirrhosis. Additionally, in recent years there is an increasing body of evidence that these channels are also involved in other relevant and prevalent liver pathological processes, such as non-alcoholic fatty liver disease, acute liver injury and portal hypertension. In parallel to these new clinical implications the available data include controversial observations. Thus, a comprehensive overview is required to better understand the functional complexity of these pores. This paper will review the most recent knowledge concerning gap junction dysfunction, with a special focus on the role of these channels in the pathogenesis of relevant clinical entities and on potential therapeutic targets that are amenable to modification by drugs.
PID Serval
serval:BIB_81949610670B
PMID
Open Access
Oui
Date de création
2019-01-23T09:45:29.371Z
Date de création dans IRIS
2025-05-20T23:36:51Z