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作 者:Na Liu Wei-Tao Yan Kun Xiong
出 处:《World Journal of Diabetes》2025年第4期1-7,共7页世界糖尿病杂志(英文)
基 金:Supported by National Natural Science Foundation of China,No.82303047,No.82372507,No.82172196 and No.32401046;Natural Science Foundation of Hunan Province,No.2022JJ40801。
摘 要:Diabetic nephropathy(DN)is a well-known microvascular complication in patients with diabetes mellitus,which is characterized by the accumulation of extracellular matrix in the glomerular and tubulointerstitial compartments,along with the hyalinization of intrarenal vasculature.DN has recently emerged as a leading cause of chronic and end-stage renal disease.While the pathobiology of other diabetic microvascular complications,such as retinopathy,is largely understood and has reasonable therapeutic options,the mechanisms and management strategies for DN remain incompletely elucidated.In this editorial,we comment on the article by Liu et al,focusing on the mechanisms underlying the detrimental impact ofβ-arrestin-2 on the kidneys in the context of DN.The authors suggest that inhibitingβ-arrestin-2 could alleviate renal damage through suppressing apoptosis of glomerular endothelial cells(GENCs),highlightingβ-arrestin-2 as a promising therapeutic target for DN.The study proposed thatβ-arrestin-2 triggers endoplasmic reticulum(ER)stress via the ATF6 signaling pathway,thereby promoting GENC apoptosis and exacerbating DN progression.Given the novel and crucial role ofβ-arrestin-2 in ER stress-related DN,it is imperative to further exploreβ-arrestin-2,its roles in ER stress and the potential therapeutic implications in DN.
关 键 词:Diabetes mellitus Diabetic nephropathy β-arrestin-2 Endoplasmic reticulum stress ATF6 signaling pathway
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