Ischemic acute renal failure: An inflammatory disease?
Ischemic acute renal failure: An inflammatory disease?
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DOI：
10.1111/j.1523-1755.2004.761_2.x
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发表时间：
2004-08-01
影响因子：
19.6
通讯作者：
Zuk, A
中科院分区：
文献类型：
--
作者：
Bonventre, JV;Zuk, A
炎症在缺血所致急性肾功能衰竭的病理生理学中起主要作用。在这篇综述中，我们讨论了内皮细胞、上皮细胞和白细胞在炎症反应中的作用。本文就细胞因子/趋化因子在损伤和恢复期的作用作一综述。小鼠肾脏通过预先暴露于缺血或尿路梗阻而受到保护的能力被讨论为一个潜在的可模仿的模型，因为我们正在寻找将服务于保护肾脏免受损伤的药理药物。了解缺血性肾损伤中普遍存在的炎症反应将有助于确定治疗干预的分子靶点。
Inflammation plays a major role in the pathophysiology of acute renal failure resulting from ischemia. In this review, we discuss the contribution of endothelial and epithelial cells and leukocytes to this inflammatory response. The roles of cytokines/chemokines in the injury and recovery phase are reviewed. The ability of the mouse kidney to be protected by prior exposure to ischemia or urinary tract obstruction is discussed as a potential model to emulate as we search for pharmacologic agents that will serve to protect the kidney against injury. Understanding the inflammatory response prevalent in ischemic kidney injury will facilitate identification of molecular targets for therapeutic intervention.