The inflammatory response to ischemic acute kidney injury: a result of the ‘right stuff’ in the ‘wrong place’?
| Autor: | Jianlin Chen, Martin Senitko, John R. Hartono, Christopher Y. Lu |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Necrosis
Apoptosis Inflammation Kidney HMGB1 RAGE (receptor) Proinflammatory cytokine Antigens CD Ischemia Internal Medicine Humans Medicine biology business.industry Toll-Like Receptors Acute kidney injury Kidney metabolism Acute Kidney Injury medicine.disease Nephrology Immunology biology.protein TLR4 Mitogen-Activated Protein Kinases Poly(ADP-ribose) Polymerases medicine.symptom business |
| Zdroj: | Current Opinion in Nephrology and Hypertension. 16:83-89 |
| ISSN: | 1062-4821 |
| DOI: | 10.1097/mnh.0b013e3280403c4e |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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