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肝再生增强因子在急性肾损伤中的研究进展

Research progress of augmenter of liver regeneration in acute kidney injury
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摘要 肝再生增强因子(augmenter of liver regeneration,ALR)是一种新近发现的细胞因子,具有促进肝脏再生和受损肝脏细胞增殖等多种生物功能。在肾脏组织内,ALR主要表达于肾髓质区的髓襻、集合管和远曲小管上皮细胞的胞浆内,在肾小球和皮质区小管细胞表达低。缺血、缺氧、中毒、炎症刺激等各种刺激可以诱导ALR在近端小管再生的上皮细胞内和皮质损伤区表达,参与了修复过程。在急性肾损伤(acute kidney injury,AKI)时,外源性ALR可以通过抑制肾小管上皮细胞凋亡、促进肾小管上皮细胞增殖、抑制炎症细胞活动等多种途径保护肾小管上皮细胞,进而降低对肾脏的损伤。该文通过复习ALR的基本特点以及AKI发病机制,并通过梳理近年来探讨ALR与AKI的相关文献,概括ALR在AKI中的作用机制特点,为探讨今后深入ALR在肾脏的研究提供知识储备和方向参考。 Augmenter of liver regeneration(ALR)is a newly discovered cytokine that can promote liver regeneration and proliferation of damaged liver cells.In the renal tissue,ALR is mainly expressed in the cytoplasm of the medullary loops,collecting ducts and distal convoluted tubules in the renal medulla,and is low in the glomerular and cortical tubules.Various stimulation,such as ischemiacal,hypoxia,poisoning and inflammatory stimulation,can induce the expression of ALR in the epithelial cells of proximal tubule regeneration and the damaged areas of cortex,and participate in the repair process.Current studies have found that in acute kidney injury(AKI),exogenous ALR can protect renal tubular epithelial cells by inhibiting apoptosis of renal tubular epithelial cells,promoting proliferation of renal tubular epithelial cells,inhibiting the activities of inflammatory cells,and promoting the reduction of renal injury.This paper intends to review the basic characteristics of ALR and the pathogenesis of AKI,summarize the characteristics of the mechanism of ALR in AKI by combing the relevant literature on ALR and AKI in recent years,and provide knowledge reserve and direction reference for the in-depth study of ALR in kidney in the future.
作者 余丹 蒲涛 YU Dan;PU Tao(Department of Urology,Affiliated Hospital of Zunyi Medical University,Zunyi,Guizhou 563099,P.R.China)
出处 《华西医学》 CAS 2021年第9期1310-1314,共5页 West China Medical Journal
基金 国家自然科学基金(81860139)。
关键词 肝再生增强因子 急性肾损伤 缺血/再灌注损伤 炎症 线粒体 Augmenter of liver regeneration Acute kidney injury Ischemia/reperfusion injury Inflammatory Mitochondria
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