Effect of miR-21 on Renal Fibrosis Induced by Nano-SiO2 in Diabetic Nephropathy Rats via PTEN/AKT Pathway

PTEN公司 蛋白激酶B PI3K/AKT/mTOR通路 纤维化 癌症研究 张力素 发病机制 生物 肾脏疾病 糖尿病肾病 内分泌学 医学 信号转导 内科学 细胞生物学
作者
Jia Guo
出处
期刊:Journal of Nanoscience and Nanotechnology [American Scientific Publishers]
卷期号:21 (2): 1079-1084 被引量:11
标识
DOI:10.1166/jnn.2021.18631
摘要

MicroRNAs are a type of non-coding single-stranded RNA that can mediate target mRNA degradation or inhibit target mRNA translation, thereby regulating target gene expression and have an important role in physiological and pathological processes. At present, miRs have been confirmed to be closely related to kidneys and kidney diseases, and have been involved in the occurrence, development and prognosis of renal fibrosis. Now we review the research progress of miRs in renal fibrosis in recent years, and provide references for the future diagnosis and treatment of renal fibrosis. The incidence of diabetic nephropathy (DN) is increasing year by year, the pathogenesis is complicated, and renal fibrosis occurs during the progress of the disease, which is very difficult to treat. The protein encoded by the PTEN gene has lipid phosphatase and protein phosphatase activity and is the PTEN/AKT and FAK pathway important negative regulators. It can play an anti-fibrotic effect by negatively regulating the PTEN/AKT pathway. Studies show that during the pathogenesis of DN, the expression of PTEN protein is reduced, and the PI3K/AKT pathway is activated to exert multiple fibrotic effects, but affect PTEN. The regulatory factors of expression are still not clear; moreover, the specific mechanism of the decrease in PTEN protein expression in DN pathogenesis. Therefore, this study intends to Intervention of the expression level of miRs in renal tissues, to study its regulation of PTEN and its effect on renal fibrosis, and at the same time, observe the effects on renal tubular epithelial cell phenotype and fibrotic lesions under high glucose conditions by up-regulating and down-regulating PTEN expression. Further elucidate the pathogenesis of DN renal fibrosis, and explore new effective targets for the prevention and treatment of DN.

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