Protein kinase C beta deficiency increases glucose-mediated peritoneal damage via M1 macrophage polarization and up-regulation of mesothelial protein kinase C alpha

Abstract Background Peritoneal membrane (PM) damage during peritoneal dialysis (PD) is mediated largely by high glucose (HG)–induced pro-inflammatory and neo-angiogenic processes, resulting in PM fibrosis and ultrafiltration failure. We recently demonstrated a crucial role for protein kinase C (PKC)...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Nephrology, dialysis, transplantation dialysis, transplantation, 2019-06, Vol.34 (6), p.947-960
Hauptverfasser:	Balzer, Michael S, Helmke, Alexandra, Ackermann, Martina, Casper, Janis, Dong, Lei, Hiss, Marcus, Kiyan, Yulia, Rong, Song, Timrott, Kai, von Vietinghoff, Sibylle, Wang, Le, Haller, Hermann, Shushakova, Nelli
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Chemokine CCL2 - metabolism Dialysis Solutions - metabolism Disease Models, Animal Epithelial Cells Epithelium Female Glucose - metabolism Humans Inflammation Lipopolysaccharides - pharmacology Macrophages - metabolism Mice Mice, Transgenic Neovascularization, Pathologic Omentum - metabolism Peritoneal Dialysis - adverse effects Peritoneal Fibrosis - metabolism Peritoneum - metabolism Protein Isoforms Protein Kinase C beta - deficiency Protein Kinase C-alpha - metabolism Tumor Necrosis Factor-alpha - metabolism Up-Regulation
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Schreiben Sie den ersten Kommentar!