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Role of p53/miR-155-5p/sirt1 loop in renal tubular injury of diabetic kidney disease

机译:p53 / miR-155-5p / sirt1环在糖尿病肾病肾小管损伤中的作用

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摘要

BackgroundDiabetic kidney disease is a renal microvascular disease caused by diabetes, known as one of the most serious and lethal complications of diabetes. Early renal hypertrophy is the main pathological feature, which gradually leads to the deposition of glomerular extracellular matrix and tubulointerstitial fibrosis, eventually developing irreversible structural damage to the kidneys. Autophagy is a cell self-homeostatic mechanism that is activated under stress conditions and may serve as a protective response to the survival of renal fibrogenic cells. MicroRNA (miRNA) network may be involved in the regulation of fibrosis. The purpose of this study is to assess how miRNAs regulate diabetic kidney disease and autophagy and fibrosis in renal proximal tubular cells under high glucose conditions.
机译:背景技术糖尿病性肾脏疾病是由糖尿病引起的肾脏微血管疾病,被称为糖尿病的最严重和致命的并发症之一。早期的肾脏肥大是主要的病理特征,逐渐导致肾小球细胞外基质的沉积和肾小管间质纤维化,最终对肾脏产生不可逆的结构损伤。自噬是一种细胞自我平衡机制,可在应激条件下被激活,并可作为对肾纤维化细胞存活的保护性反应。 MicroRNA(miRNA)网络可能参与纤维化的调节。这项研究的目的是评估在高葡萄糖条件下,miRNA如何调节糖尿病性肾脏疾病以及肾近端肾小管细胞的自噬和纤维化。

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