The mTOR/p70S6K1 signaling pathway in renal fibrosis of children with immunoglobulin A nephropathy

Aim: The purpose of this study was to explore whether mTOR/p70S6K1 signaling is activated in renal fibrosis of immunoglobulin A nephropathy.Methods: Seventy-two children with immunoglobulin A nephropathy were divided into three groups according to their clinical features and pathological grades. Six normal renal specimens were included in the control group. The expression levels of angiotensin II, mTOR, p70S6K1, E-cadherin, and α-smooth muscle actin in renal tissues were determined by immunohistochemistry method, the potential correlations of these indexes and relationship between these indexes and the clinicopathological indexes were analyzed.Results: Compared to the control group, the expression levels of angiotensin II, mTOR, p70S6K1, and α-smooth muscle actin were significantly higher and the expression levels of E-cadherin were lower both in glomeruli and tubulointerstitium of immunoglobulin A nephropathy children. And the most significant differences were found in the nephrotic syndrome group and pathological grade IV group. In immunoglobulin A nephropathy renal tissues, the expression levels of angiotensin II in glomeruli and tubulointerstitium were both positively correlated with the expression levels of mTOR and α- smooth muscle actin, and negatively correlated with the expression levels of E-cadherin.Conclusion: The mTOR/p70S6K1 signaling was activated in renal tissues of children with immunoglobulin A nephropathy, and future studies will need to address the mechanism of mTOR/p70S6K1 signaling in the progress of renal fibrosis in immunoglobulin A nephropathy.