PDF(Pubmed)
Abstract：
Kidney transplantation offers a longer life expectancy and a better quality of life than dialysis to patients with end-stage kidney disease. Ischemia-reperfusion injury (IRI) is thought to be a cornerstone in delayed or reduced graft function and increases the risk of rejection by triggering the immunogenicity of the organ. IRI is an unavoidable event that happens when the blood supply is temporarily reduced and then restored to an organ. IRI is the result of several biological pathways, such as transcriptional reprogramming, apoptosis and necrosis, innate and adaptive immune responses, and endothelial dysfunction. Tubular cells mostly depend on fatty acid (FA) β-oxidation for energy production since more ATP molecules are yielded per substrate molecule than glucose oxidation. Upon ischemia-reperfusion damage, the innate and adaptive immune system activates to achieve tissue clearance and repair. Several cells, cytokines, enzymes, receptors, and ligands are known to take part in these events. The complement cascade might start even before organ procurement in deceased donors. However, additional experimental and clinical data are required to better understand the pathogenic events that take place during this complex process.
摘要：
对于终末期肾病患者，肾移植比透析提供更长的预期寿命和更好的生活质量。缺血再灌注损伤（IRI）被认为是延迟或降低移植物功能的基石，并通过触发器官的免疫原性增加了排斥的风险。IRI是一种不可避免的事件，当血液供应暂时减少然后恢复到器官时发生。IRI是几种生物学途径的结果，例如转录重编程，凋亡和坏死，先天和适应性免疫反应，和内皮功能障碍。管状细胞主要依靠脂肪酸（FA）β-氧化来产生能量，因为每个底物分子比葡萄糖氧化产生更多的ATP分子。在缺血再灌注损伤时，先天和适应性免疫系统激活以实现组织清除和修复。几个细胞，细胞因子,酶，受体,和配体已知参与这些事件。甚至在已故捐赠者的器官采购之前，补体级联就可能开始。然而,需要更多的实验和临床数据来更好地了解在这一复杂过程中发生的致病事件.
