ArticleMolecular and cellular biochemistry2025
PACS2/PKCα/NOX4 pathway damaged the renal vascular endothelial barrier by promoting ROS production in diabetic nephropathy mice.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Letter to the Editors-correspondence.Molecular and cellular biochemistry · 2026Article
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10 authors.
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Abstract
Renal vascular endothelial barrier dysfunction plays an important role in the pathogenesis of diabetic nephropathy (DN). Reactive oxygen species (ROS) contribute to barrier dysfunction in various aspects of diabetes. Phosphofurin acidic cluster sorting protein 2 (PACS2) is related to the ROS production, but the specific signaling pathway in endothelial cells remains unclear. In this study, we explored the mechanistic function of PACS2 and its downstream PKCα/NOX4 signaling pathway in endothelial barrier damage in DN. A significant upregulation of PACS2 expression was observed in human umbilical vein endothelial cells treated with high glucose and palmitic acid and glomerular endothelial cells derived from STZ + HFD-induced DN mice. SiRNA-mediated silencing or knockdown of PACS2 reversed the impaired vascular barrier function in vivo and in vitro. Furthermore, the inhibition of PACS2 significantly downregulated the protein expression of PKCα and NOX4 protein and the production of ROS in endothelial cells. Collectively, our findings indicate that the PACS2/PKCα/NOX4 signaling pathway may participate in the pathogenesis of DN by regulating vascular endothelial barrier function.
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