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Pitavastatin suppresses hyperglycaemia‐induced podocyte injury via bone morphogenetic protein‐7 preservation

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Clinical and Experimental Pharmacology and Physiology

Published online on


Podocytes form the essential components of the glomerular filtration barrier and play a critical role in diabetic nephropathy. Recent evidence suggests that HMG‐CoA reductase inhibitors (statins) exert renoprotective effects. We investigated whether pitavastatin directly suppresses hyperglycaemia‐induced podocyte injury using cultured podocytes and, if so, the mechanism of the beneficial effects. Cultured podocytes were exposed to media containing normal (NG; 5 mmol/L) or high (HG; 25 mmol/L) glucose for 1 week. HG increased the lethal injury of podocytes and disruption of F‐actin fibers, and reduced the mRNA expression of novel podocyte markers, synaptopodin and Wilms tumor‐1 (WT‐1), in association with decreased bone morphogenetic protein‐7 (BMP‐7) expression. Pitavastatin (100 nmol/L) reduced podocyte injury and restored the mRNA expression of synaptopodin and WT1; however, these protective effects were abolished by BMP‐7 siRNA. Additionally, pitavastatin suppressed HG‐induced Rho kinase activation, as assessed by the phosphorylation level of myosin phosphatase targeting subunit 1 (MYTP1), and C3 exotoxin, a Rho inhibitor, mimicked the effect of pitavastatin on BMP‐7 preservation. Pitavastatin attenuates hyperglycaemia‐induced podocyte injury via Rho‐Rho kinase‐dependent BMP‐7 preservation.