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

Journal of Translational Medicine
Yue WangYao-Ming Xue

Abstract

Diabetic 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. Human renal proximal tubular (HK-2) cells were exposed to high glucose in vitro. Bioinformatic analysis was used to select the candidate gene for potential target regulation of miR-155, Sirt1. ATG5, ATG7 is the key to autophagosome formation, regulated by Sirt1. p53 regulates miR-155 expression as a transcription factor. MiR-155 overexpression and inhibition were achieved by transfection of miR-155 mimic and inhibit to evaluate its effect on Si...Continue Reading

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Citations

Nov 30, 2019·Frontiers in Pharmacology·Jose Luis Morgado-PascualMarta Ruiz-Ortega
Jun 27, 2020·Oxidative Medicine and Cellular Longevity·Wanfen ZhangTongqiang Liu
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Methods Mentioned

BETA
transfection
PCR
Chip
acetylation

Software Mentioned

Excel
TargetScan

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