医学
急性肾损伤
病理生理学
缺血
肾
再灌注损伤
氧化应激
缺氧(环境)
炎症
肾功能
生物信息学
心脏病学
内科学
生物
化学
有机化学
氧气
作者
Maryam Malek,Mehdi Nematbakhsh
出处
期刊:PubMed
日期:2015-01-01
卷期号:4 (2): 20-7
被引量:494
标识
DOI:10.12861/jrip.2015.06
摘要
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.
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