High glucose activates PKC-ζ and NADPH oxidase through autocrine TGF-β₁ signaling in mesangial cells

Abstract

CI. High glucose activates PKC-and NADPH oxidase through autocrine TGF-␤ 1 signaling in mesangial cells.

Advanced oxidation protein products induce mesangial cell perturbation through PKC-dependent activation of NADPH oxidase

“…Previous study has also shown that exposure of preglomerular vascular smooth muscle cells to TGF-␤1 triggers a rapid increase in ROS that is inhibited by NADPH oxidase inhibitors (33). Consistent with other studies that were conducted in MCs stimulated by a high concentration of glucose (16,42), our data showed that AOPPs-induced activation of PKC and NADPH oxidase could be partly inhibited by neutralizing the effect of TGF-␤1. Therefore, it seems reasonable to assume that in addition to O 2 Ϫ produced by AOPPs-activated NADPH oxidase, newly synthesized TGF-␤1, as a downstream signaling event, can further activate PKC␣ and NADPH oxidase to produce ROS (14).…”

Oxidative and Nitrosative Stress and Progression of Diabetic Nephropathy in Type 2 Diabetes

“…Hyperglycemia is thought to be closely associated with increased oxidative and nitrosative stress, which can trigger the development of diabetic nephropathy. Hyperglycemia stimulates the production of advanced glycosylated end products, activates NADPH oxidase through protein kinase C, and enhances the polyol pathway, thus leading to increased superoxide anion formation [22,23,24]. Certainly, mRNA expression of the NADPH subunit and the urinary excretion of 8-OHdG, which is a marker of oxidative DNA damage, were significantly increased in our diabetic model.…”

Diabetic Renal Injury Induced in Experimental Rats-Role of Curcuminoids as Probable Therapeutic Agent

“…IV. DISCUSSION As reported before hyperglycemia can activate polyol pathway, NADPH oxidase leading to increased oxidative stress, endothelial dysfunction, proliferation of vascular smooth muscle cells and induction of cellular damage [19][20][21].…”