Activation of Pannexin-1 channels causes cell dysfunction and damage in mesangial cells derived from angiotensin II-exposed mice.
ATP
hypertensive nephropathy
inflammation
intracellular Ca2+
panx1
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2024
2024
Historique:
received:
17
02
2024
accepted:
25
03
2024
medline:
25
4
2024
pubmed:
25
4
2024
entrez:
25
4
2024
Statut:
epublish
Résumé
Chronic kidney disease (CKD) is a prevalent health concern associated with various pathological conditions, including hypertensive nephropathy. Mesangial cells are crucial in maintaining glomerular function, yet their involvement in CKD pathogenesis remains poorly understood. Recent evidence indicates that overactivation of Pannexin-1 (Panx1) channels could contribute to the pathogenesis and progression of various diseases. Although Panx1 is expressed in the kidney, its contribution to the dysfunction of renal cells during pathological conditions remains to be elucidated. This study aimed to investigate the impact of Panx1 channels on mesangial cell function in the context of hypertensive nephropathy. Using an Ang II-infused mouse model and primary mesangial cell cultures, we demonstrated that
Identifiants
pubmed: 38660621
doi: 10.3389/fcell.2024.1387234
pii: 1387234
pmc: PMC11041381
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1387234Informations de copyright
Copyright © 2024 Lucero, Navarro, Barros-Osorio, Cáceres-Conejeros, Orellana and Gómez.
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.