Gap junctions in liver disease: Implications for pathogenesis and therapy.

Détails

ID Serval
serval:BIB_81949610670B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Gap junctions in liver disease: Implications for pathogenesis and therapy.
Périodique
Journal of hepatology
Auteur(s)
Hernández-Guerra M., Hadjihambi A., Jalan R.
ISSN
1600-0641 (Electronic)
ISSN-L
0168-8278
Statut éditorial
Publié
Date de publication
04/2019
Peer-reviewed
Oui
Volume
70
Numéro
4
Pages
759-772
Langue
anglais
Notes
Publication types: Journal Article ; Review
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.
Mots-clé
Cirrhosis, Connexins, Gap junctions, Hemichannels, Intercellular communication, Liver
Pubmed
Open Access
Oui
Création de la notice
23/01/2019 11:45
Dernière modification de la notice
21/08/2019 6:15
Données d'usage