The inflammatory response to ischemic acute kidney injury: a result of the ‘right stuff’ in the ‘wrong place’? Curr Opin Nephrol Hypertens

Department of Internal Medicine, Nephrology Division, UT Southwestern Medical Center, Dallas, Texas 63110, USA.
Current Opinion in Nephrology and Hypertension (Impact Factor: 3.86). 04/2007; 16(2):83-9. DOI: 10.1097/MNH.0b013e3280403c4e
Source: PubMed


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.
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.
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.

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