对缺血性急性肾损伤的炎症反应：是“正确的物质”出现在“错误的位置”的结果吗？
The inflammatory response to ischemic acute kidney injury: a result of the 'right stuff' in the 'wrong place'?
作者信息
Lu Christopher Y, Hartono John, Senitko Martin, Chen Jianlin
机构信息
Department of Internal Medicine, Nephrology Division, UT Southwestern Medical Center, Dallas, Texas 63110, USA.
出版信息
Curr Opin Nephrol Hypertens. 2007 Mar;16(2):83-9. doi: 10.1097/MNH.0b013e3280403c4e.
PURPOSE OF REVIEW
Ischemic acute kidney injury may be exacerbated by an inflammatory response. How injury elicits inflammation remains a major question in understanding acute kidney injury. The present review examines the hypothesis that molecules released by injured cells elicit inflammation.
RECENT FINDINGS
After necrotic death, intracellular molecules find their way into the extracellular space. These molecules include heat shock proteins and HMGB1. Receptors for these proteins include TLR4, TLR2, CD91 and RAGE. These proinflammatory mechanisms may be so useful that nature has evolved mechanisms for programming necrotic death via poly(ADP-ribose) polymerase and cyclophilin D. In addition, apoptosis may also elicit inflammation.
SUMMARY
The concepts discussed in this review are important for clinical medicine. Drugs and genetic manipulation may ameliorate ischemic kidney injury by regulating the inflammatory response to cell injury.
综述目的
缺血性急性肾损伤可能会因炎症反应而加重。损伤如何引发炎症仍是理解急性肾损伤的一个主要问题。本综述探讨了受损细胞释放的分子引发炎症这一假说。
最新发现
细胞坏死死亡后，细胞内分子进入细胞外空间。这些分子包括热休克蛋白和高迁移率族蛋白B1。这些蛋白的受体包括Toll样受体4、Toll样受体2、CD91和晚期糖基化终末产物受体。这些促炎机制可能非常有用，以至于自然界进化出了通过聚（ADP - 核糖）聚合酶和亲环素D编程坏死死亡的机制。此外，细胞凋亡也可能引发炎症。
总结
本综述中讨论的概念对临床医学很重要。药物和基因操作可能通过调节对细胞损伤的炎症反应来改善缺血性肾损伤。
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