Abstract：Objective: To establish a rat model of diabetic kidney disease (DKD) and explore the mechanism by which METTL3 regulates DKD.Methods: After 7 days of adaptive feeding, SD rats were randomly divided into four groups: normal control group (Control group), DKD model group (DKD group), DKD model + METTL3 interference control group (DKD+NC group), and DKD model + METTL3 interference group (DKD+siMETTL3 group), with 8 rats in each group. After modeling, blood specimens and kidney tissues were collected, and levels of fasting blood glucose (FBG), blood urea nitrogen (BUN), 24-hour urine protein (UTP), gene expression of miR-126 using RT-qPCR, expression of TGF-β1 using ELISA, and protein levels of METTL3, smad2, smad3, and smad7 using Western blotting were analyzed by a fully automatic biochemical analyzer. Results: Compared to the control group, the DKD group showed significant increases in FBG, BUN, UTP, TGF-β1, METTL3, smad2, and smad3 (P<0.05), and significant decreases in body weight, miR-126, and smad7 (P<0.05). When compared to the DKD group, the DKD+siMETTL3 group exhibited significant decreases in FBG, BUN, UTP, TGF-β1, METTL3, smad2, and smad3 (P<0.05), and significant increases in body weight, miR-126, and smad7 (P<0.05). Conclusion: METTL3 can mediate the progression of DKD by regulating miR-126 and TGF-β/smad pathway.
张静, 任荣, 帕提古丽·阿斯讨拜. METTL3调控miR-126介导TGF-β/Smad信号通路影响糖尿病肾病的机制研究[J]. 河北医学, 2024, 30(3): 377-380.
ZHANG Jing, REN Rong, Patiguli·ASITANBAI. Mechanistic Study on the Regulation of Diabetes Kidney Disease by METTL3 through the miR-126-Mediated TGF-β/Smad Signaling Pathway. HeBei Med, 2024, 30(3): 377-380.
2024, Vol. 30 
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