摘要
肾脏缺血再灌注损伤( IRKI)是一个复杂的病理生理事件,这是急性肾损伤最常见的原因。 IRKI的关键特征是肾小球滤过率降低,这意味着一个潜在的损伤血流动力学的调节。近几十年来,有说服力的证据阐明了急性肾损伤的分子和病理事件,揭示了缺血/再灌注损伤的作用,氧化应激、细胞凋亡、炎症、纤维化和激活不同信号通路的基因表达的变化。炎症的级联事件是 IRKI的关键介质,包括炎症过程,激活先天免疫的动员补充。氧化应激代表增加的各种自由基的存在,不能缓冲的抗氧化能力,其中包括的酶和非酶成分。缺血再灌注肾组织损伤是膜脂质过氧化、蛋白质和DNA的氧化损伤,导致细胞凋亡和坏死的结果。许多研究表明,增强抗氧化防御机制对肾脏组织有保护作用,这是很明显的。近年来,在 IRKI发生热休克蛋白和RNA的重要性已显示有前途的迹象表明,在未来他们可以作为诊断标志物或治疗靶点。显示在全球基因表达的显著变化,为irki基本认识和临床管理潜力巨大。肾移植患者的临床结局的 IRKI分子病理学更好的理解有进一步进展。
关键词: 肾脏缺血再灌注损伤、炎症、氧化应激、抗氧化、线粒体、热休克蛋白、RNA,基因表达。
Current Medicinal Chemistry
Title:Molecular Dissection of Renal Ischemia-Reperfusion: Oxidative Stress and Cellular Events
Volume: 23 Issue: 19
Author(s): Branislav Rovcanin, Branislava Medic, Gordana Kocic, Tatjana Cebovic, Marko Ristic, Milica Prostran
Affiliation:
关键词: 肾脏缺血再灌注损伤、炎症、氧化应激、抗氧化、线粒体、热休克蛋白、RNA,基因表达。
摘要: Ischemic reperfusion kidney injury (IRKI) is a complex pathophysiological event, which is the most common cause of the acute kidney injury. The key characteristic of IRKI is a reduction in glomerular filtration rate, which implies an underlying impairment in hemodynamic regulation. In recent decades, convincing evidence illuminated the molecular and pathological events in the acute kidney injury, revealing the role of ischemia/reperfusion, oxidative stress, apoptosis, inflammation, fibrosis and changes in gene expression which activate different signaling pathways. The cascade of inflammation events is a key mediator of IRKI, which includes the inflammation process, complement activation and mobilization of innate immunity. Oxidative stress represents the increased presence of various free radicals that cannot be buffered by the antioxidant capacity which comprises of enzymatic and non-enzymatic components. Renal tissue injury during ischemia/reperfusion comes as a result of membrane lipids peroxidation, oxidative damage of proteins and DNA and results in apoptosis and necrosis. It is evident from many studies that augmentation of the antioxidant defense mechanisms has a protective role on kidney tissue. In recent years, the importance of heat-shock proteins and MicroRNAs in the pathogenesis of IRKI has been revealed and there are promising indications that in future they could serve as diagnostic biomarkers or therapeutic targets. Striking changes in global gene expression were shown, providing a great potential for fundamental understanding and clinical management of IRKI. The clinical outcome among patients with kidney transplantation will have the furthermost advance from the better understanding of the underlying molecular pathology of IRKI.
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Branislav Rovcanin, Branislava Medic, Gordana Kocic, Tatjana Cebovic, Marko Ristic, Milica Prostran , Molecular Dissection of Renal Ischemia-Reperfusion: Oxidative Stress and Cellular Events, Current Medicinal Chemistry 2016; 23 (19) . https://dx.doi.org/10.2174/0929867323666160112122858
DOI https://dx.doi.org/10.2174/0929867323666160112122858 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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