关键词: Autophagy Chronic kidney disease Energy restriction Energy restriction mimetics Mammalian target of rapamycin pathway

Mesh : Adenosine Kinase / metabolism Animals Caloric Restriction DNA Repair / physiology Disease Progression Energy Intake / physiology Humans Kidney Organelle Biogenesis Oxidative Stress / physiology Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / metabolism Protective Factors Renal Insufficiency, Chronic / diet therapy metabolism Sirtuin 1 / metabolism

来  源:   DOI:10.1017/S000711452000358X   PDF(Sci-hub)

Abstract:
Energy restriction (ER) has anti-ageing effects and probably protects from a range of chronic diseases including cancer, diabetes and chronic kidney disease (CKD). Specifically, ER has a positive impact on experimental kidney ageing, CKD (diabetic nephropathy, polycystic kidney disease) and acute kidney injury (nephrotoxic, ischaemia-reperfusion injury) through such mechanisms as increased autophagy, mitochondrial biogenesis and DNA repair, and decreased inflammation and oxidative stress. Key molecules contributing to ER-mediated kidney protection include adenosine monophosphate-activated protein kinase, sirtuin-1 and PPAR-γ coactivator 1α. However, CKD is a complex condition, and ER may potentially worsen CKD complications such as protein-energy wasting, bone-mineral disorders and impaired wound healing. ER mimetics are drugs, such as metformin and Na-glucose co-transporter-2 which mimic the action of ER. This review aims to provide comprehensive data regarding the effect of ER on CKD progression and outcomes.
摘要:
能量限制(ER)具有抗衰老作用,并可能防止一系列慢性疾病,包括癌症,糖尿病和慢性肾脏疾病(CKD)。具体来说,ER对实验性肾脏老化有积极影响,CKD(糖尿病肾病,多囊肾病)和急性肾损伤(肾毒性,缺血再灌注损伤)通过自噬增加等机制,线粒体生物发生和DNA修复,减少炎症和氧化应激。促进ER介导的肾脏保护的关键分子包括一磷酸腺苷激活的蛋白激酶,沉默酶-1和PPAR-γ共激活因子1α。然而,CKD是一个复杂的条件,内质网可能会加重CKD并发症,如蛋白质能量消耗,骨矿物质紊乱和伤口愈合受损。ER模拟物是药物,如二甲双胍和Na-葡萄糖共转运蛋白-2,其模拟ER的作用。这篇综述旨在提供有关ER对CKD进展和结局影响的全面数据。
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