%0 Journal Article
%T Hyperglycemia activates the renin
%A Chung-Ming Chen
%A Hsiu-Chu Chou
%A Shu-Hui Juan
%J Journal of the Renin
%@ 1752-8976
%D 2018
%R 10.1177/1470320318803009
%X The renin每angiotensin system and epithelial每mesenchymal transition play crucial roles in the development of kidney fibrosis. The connection between the renin每angiotensin system and transforming growth factor-汕 in epithelial每mesenchymal transition remains largely unknown. We assessed oxidative stress, cytokine levels, renal morphology, profibrotic growth factor and renin每angiotensin system component expression, and cell-specific E- and N-cadherin expression in the kidneys of gerbils with streptozotocin-induced diabetes mellitus. Animals in the experimental group received an intraperitoneal injection of streptozotocin to induce diabetes. The diabetic gerbil kidneys presented kidney injury, which was manifested as distorted glomeruli, necrosis of tubular cells, dilated tubular lumen, and brush border loss. Additionally, the diabetic gerbil kidneys exhibited significantly higher expressions of 8-hydroxy-2∩-deoxyguanosine, nuclear factor-kB, toll-like receptor 4, tumor necrosis factor-汐, transforming growth factor-汕, connective tissue growth factor, 汐-smooth muscle actin, and N-cadherin and higher collagen deposition than did the control gerbil kidneys. Compared with the control kidneys, the diabetic gerbil kidneys exhibited significantly lower E-cadherin expression. These epithelial每mesenchymal transition characteristics were associated with an increase in renin每angiotensin system expression in the diabetic gerbils. We demonstrate that hyperglycemia activated the renin每angiotensin system, induced epithelial每mesenchymal transition, and contributed to kidney fibrosis in an experimental diabetes mellitus model
%K Connective tissue growth factor
%K cadherin
%K nuclear factor-百B
%K toll-like receptor
%K transforming growth factor-汕
%U https://journals.sagepub.com/doi/full/10.1177/1470320318803009