摘要
肾缺血再灌注损伤(IRI)是导致急性肾损伤(AKI)的主要原因之一,可能导致慢性肾脏病。在过去的5个月里,AKI的高死亡率没有改变。ADS因未识别、肾毒素暴露、诊断延迟及缺乏具体干预.。补体激活在IRI诱导的AKI中起着重要作用,因为它与i有关。免疫,炎症,细胞死亡和组织修复。然而,作为替代途径唯一的正调节因子,补体蛋白在iri诱导的aki中的作用还没有得到很好的界定。D.评估的动态变化及其机制激活补体在体外和体内模型,缺氧/复氧和R挑战备解素的焦点肾IRI。本文从免疫、损伤和修复的角度讨论了与hmb 1和caspase-3有关的细胞凋亡和炎症介质的多种作用。AKI的后期阶段。本文还讨论了非补体激活作用,并探讨了与基因型改变有关的调节作用。在一起的话,这股力量t提供了新的机制见解,有助于IRI诱导的AKI的及时诊断和特异性干预。
关键词: 补体激活,缺血再灌注损伤,肾,产权,组织修复,急性肾损伤。
Current Gene Therapy
Title:Role of Complement Properdin in Renal Ischemia-Reperfusion Injury
Volume: 17 Issue: 6
关键词: 补体激活,缺血再灌注损伤,肾,产权,组织修复,急性肾损伤。
摘要: Renal Ischemia-Reperfusion Injury (IRI) is one of the main causes of Acute Kidney Injury (AKI), and may lead to chronic kidney disease. The high mortality rate of AKI has not changed in the last 5 decades due to non-recognition, nephrotoxin exposure, delayed diagnosis and lack of specific intervention. Complement activation plays important roles in IRI-induced AKI because of its association with immunity, inflammation, cell death and tissue repair. Nevertheless, the role of complement properdin, the sole positive regulator of the alternative pathway, in IRI-induced AKI has not been well defined. This review evaluates the dynamic changes and underlying mechanisms of complement activation with a focus on properdin in both in vitro and in vivo models challenged by hypoxia/ reoxygenation and renal IRI. The multiple actions of properdin associated with HMGB1 and caspase-3, apoptosis and inflammation mediators, are discussed in the context of immunity, injury and repair at both the early and later stages of AKI. The complement activation-independent role of properdin and the effect of modulating properdin with or without genotype alteration are also addressed. Taking together, these might provide new mechanistic insights that potentially benefit timely diagnosis and specific intervention of IRI-induced AKI.
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Role of Complement Properdin in Renal Ischemia-Reperfusion Injury, Current Gene Therapy 2017; 17 (6) . https://dx.doi.org/10.2174/1566523218666180214093043
DOI https://dx.doi.org/10.2174/1566523218666180214093043 |
Print ISSN 1566-5232 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5631 |
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