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- W2413773008 abstract "Abstract Pharmacological blockade of the N- and L-type calcium channel lessens renal injury in kidney disease patients. The significance of specific blockade of α1 subunit of N-type calcium channel, Ca v 2.2, in diabetic nephropathy, however, remains to be clarified. To examine functional roles, we mated Ca v 2.2 −/− mice with db/db (diabetic) mice on the C57BLKS background. Ca v 2.2 was localized in glomeruli including podocytes and in distal tubular cells. Diabetic Ca v 2.2 −/− mice significantly reduced urinary albumin excretion, glomerular hyperfiltration, blood glucose levels, histological deterioration and systolic blood pressure (SBP) with decreased urinary catecholamine compared to diabetic Ca v 2.2 +/+ mice. Interestingly, diabetic heterozygous Ca v 2.2 +/− mice also decreased albuminuria, although they exhibited comparable systolic blood pressure, sympathetic nerve activity and creatinine clearance to diabetic Ca v 2.2 +/+ mice. Consistently, diabetic mice with cilnidipine, an N-/L-type calcium channel blocker, showed a reduction in albuminuria and improvement of glomerular changes compared to diabetic mice with nitrendipine. In cultured podocytes, depolarization-dependent calcium responses were decreased by ω-conotoxin, a Ca v 2.2-specific inhibitor. Furthermore, reduction of nephrin by transforming growth factor-β (TGF-β) in podocytes was abolished with ω-conotoxin, cilnidipine or mitogen-activated protein kinase kinase inhibitor. In conclusion, Ca v 2.2 inhibition exerts renoprotective effects against the progression of diabetic nephropathy, partly by protecting podocytes." @default.
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- W2413773008 date "2016-06-07" @default.
- W2413773008 modified "2023-09-25" @default.
- W2413773008 title "Ablation of the N-type calcium channel ameliorates diabetic nephropathy with improved glycemic control and reduced blood pressure" @default.
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- W2413773008 doi "https://doi.org/10.1038/srep27192" @default.
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