Continuous glucose exposure contributes to severe ultrafiltration failure in peritoneal dialysis. In their study, Wang et al. describe a mechanistic pathway involving direct activation by glucose of mesothelial cell protein kinase C α that, when blocked, or absent in a mouse knockout model, prevents fibrosis and the associated reduction in ultrafiltration. Interestingly, this pathway involves the 3 main mechanisms of membrane injury (inflammation, neoangiogenesis, and fibrogenesis), offering a potential target for therapeutic intervention.
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