摘要
背景:慢性肾脏疾病(CKD)是一种日益影响全球数百万人的疾病,是美国第九大死因。AMP激活Protein激酶(oteinkinase,AMPK)是一种能量传感器,在细胞同质平衡中起着关键的作用。缺乏AMPK活性和自噬信号,并持续激活哺乳动物的猛禽靶CIN(MTOR)信号转导和内质网(ER)应激促进上皮间充质转换(EMT)和肾细胞凋亡,并参与CKD的发生。新兴证据演示研究表明,AMPK作为CKD病理生理基础的上述通路的调节因子。此外,AMPK的药理激活剂如二甲双胍也已被证明是有效的。肾保护作用的实验研究和改善CKD患者的临床结果。 目的:综述AMPK的肾保护作用及其作为CKD防治靶点的作用。
关键词: 激活蛋白激酶,凋亡,自噬,慢性肾脏疾病,内质网应激,上皮间充质转换,哺乳动物雷帕霉素靶点,二甲双胍。
图形摘要
Current Drug Targets
Title:AMP-activated Protein Kinase as a Drug Target in Chronic Kidney Disease
Volume: 19 Issue: 6
关键词: 激活蛋白激酶,凋亡,自噬,慢性肾脏疾病,内质网应激,上皮间充质转换,哺乳动物雷帕霉素靶点,二甲双胍。
摘要: Background: Chronic kidney disease (CKD) is a condition increasingly affecting millions of individuals worldwide and is ranked as the ninth leading cause of death in the United States. AMPactivated protein kinase (AMPK) is an energy sensor that plays a pivotal role in cellular homoeostasis. Deficiency in AMPK activity and autophagic signaling, and sustained activation of mammalian target of rapamycin (mTOR) signaling and endoplasmic reticulum (ER) stress have been shown to promote epithelial-to-mesenchymal transition (EMT) and renal cell apoptosis and contribute to CKD. Emerging evidences demonstrate that AMPK acts as a modulator of the aforementioned pathways that underpin the pathophysiology of CKD. Furthermore, pharmacological activators of AMPK such as metformin have been shown to exert renoprotective effects in experimental studies and improve clinical outcomes in patients with CKD.
Objective: The current review focuses on the nephroprotective effects of AMPK and its utility as a therapeutic target for the prevention and treatment of CKD.
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Cite this article as:
AMP-activated Protein Kinase as a Drug Target in Chronic Kidney Disease, Current Drug Targets 2018; 19 (6) . https://dx.doi.org/10.2174/1389450118666170601130947
DOI https://dx.doi.org/10.2174/1389450118666170601130947 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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