Renal ischemia/reperfusion injury; from pathophysiology to treatment.
Renal ischemia/reperfusion injury; from pathophysiology to treatment.
复制标题
DOI：
10.12861/jrip.2015.06
复制
发表时间：
2015
影响因子：
0.7
通讯作者：
Nematbakhsh M
中科院分区：
文献类型：
--
作者：
Malek M;Nematbakhsh M
缺血/再灌注损伤（IRI）是由流向特定器官的血流突然暂时受损引起的。IRI通常与对缺氧和再灌注的强烈炎症和氧化应激反应有关，这会干扰器官功能。肾脏IR诱导的急性肾损伤（阿基）导致多种损伤的高发病率和死亡率。虽然IRI的病理生理学还不完全清楚，但已经提到了导致肾衰竭的几个重要机制。在缺血性肾脏和随后的再氧合中，在再灌注阶段活性氧（ROS）的产生引发了一系列有害的细胞反应，导致炎症、细胞死亡和急性肾衰竭。更好地了解肾损伤的细胞病理生理机制将有望设计出更有针对性的治疗方法来预防和治疗损伤。本文就肾IRI的发病机制和治疗方法作一综述。
Ischemia/reperfusion injury (IRI) is caused by a sudden temporary impairment of the blood flow to the particular organ. IRI usually is associated with a robust inflammatory and oxidative stress response to hypoxia and reperfusion which disturbs the organ function. Renal IR induced acute kidney injury (AKI) contributes to high morbidity and mortality rate in a wide range of injuries. Although the pathophysiology of IRI is not completely understood, several important mechanisms resulting in kidney failure have been mentioned. In ischemic kidney and subsequent of re-oxygenation, generation of reactive oxygen species (ROS) at reperfusion phase initiates a cascade of deleterious cellular responses leading to inflammation, cell death, and acute kidney failure. Better understanding of the cellular pathophysiological mechanisms underlying kidney injury will hopefully result in the design of more targeted therapies to prevent and treatment the injury. In this review, we summarize some important potential mechanisms and therapeutic approaches in renal IRI.