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机构地区:[1]Department of Genetics and Bioinformatics,Dasman Diabetes Institute,Dasman 15400,Kuwait
出 处:《World Journal of Diabetes》2024年第9期1837-1841,共5页世界糖尿病杂志(英文版)(电子版)
基 金:Supported by the Kuwait Foundation for the Advancement of Sciences and Dasman Diabetes Institute,Kuwait,No.RACB-2021-007.
摘 要:In this editorial,we comment on the article by Wu et al published“MicroRNA-630 alleviates inflammatory reactions in rats with diabetic kidney disease by targeting toll-like receptor 4”.Diabetic kidney disease(DKD)stands as a significant complication occurring from diabetes mellitus,which contributes substantially to the morbidity and mortality rates worldwide.Renal tubular epithelial cell damage,often accompanied by inflammatory responses and mesenchymal transdifferentiation,plays a pivotal role in the progression of DKD.Despite extensive research,the intricate molecular mechanisms underlying these processes remain to be determined.Wu et al remarkable work identifies microRNA-630(miR-630)as an emerging potential regulator of cell migration,apoptosis,and autophagy,prompting investigation into its association with DKD pathogenesis.This study endeavors to elucidate the impact of miR-630 on TEC injury and the inflammatory response in DKD rats.The role of miR-630 in human DKD will be of interest for future studies.
关 键 词:Diabetic kidney disease MICRORNA MicroRNA-630 Toll-like receptor 4 INFLAMMATION
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