| Literature DB >> 15461705 |
Ganesan Ramesh1, W Brian Reeves.
Abstract
A growing body of evidence indicates that inflammatory mechanisms contribute to toxin-induced acute renal failure as well as ischemia/reperfusion injury. A role for tumor necrosis factor-alpha (TNF-alpha) in mediating the inflammatory injury in cisplatin-induced acute renal failure has recently been established. Cisplatin induces the expression of TNF-alpha and TNF receptor subtype 2 (TNFR2) within the kidney. Genetic deletion of either TNF-alpha or TNFR2 substantially reduces cisplatin-induced renal failure and also necrosis and apoptosis within the kidney. Studies will be required to determine if pharmacologic inhibition of TNF-alpha might reduce cisplatin-induced renal failure in humans.Entities:
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Year: 2004 PMID: 15461705 DOI: 10.1111/j.1523-1755.2004.09109.x
Source DB: PubMed Journal: Kidney Int Suppl ISSN: 0098-6577 Impact factor: 10.545