作者: Christopher Y Lu , John Hartono , Martin Senitko , Jianlin Chen
DOI: 10.1097/MNH.0B013E3280403C4E
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摘要: Purpose of review Ischemic acute kidney injury may be exacerbated by an inflammatory response. How elicits inflammation remains a major question in understanding injury. The present examines the hypothesis that molecules released injured cells elicit inflammation. Recent findings After necrotic death, intracellular find their way into extracellular space. These include heat shock proteins and HMGB1. Receptors for these TLR4, TLR2, CD91 RAGE. proinflammatory mechanisms so useful nature has evolved programming death via poly(ADP-ribose) polymerase cyclophilin D. In addition, apoptosis also Summary concepts discussed this are important clinical medicine. Drugs genetic manipulation ameliorate ischemic regulating response to cell