Tumor necrosis factor-alpha in cisplatin nephrotoxicity: a homebred foe?
A robust inflammatory response involving tumor necrosis factor-alpha (TNF-alpha) is induced during cisplatin nephrotoxicity. Using chimeric models, Reeves and colleagues now demonstrate that resident kidney cells, rather than infiltrating immune cells, are the major producers of TNF-alpha. Blockade of TNF-alpha attenuates inflammation and associated kidney injury.
Dong
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Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA. zdong@mail.mcg.edu
Atherton
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D000818:Animals; D000970:Antineoplastic Agents / Q000009:adverse effects* / Q000494:pharmacology; D002678:Chimera; D002945:Cisplatin / Q000009:adverse effects* / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D008954:Models, Biological; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics / Q000378:metabolism; D051437:Renal Insufficiency / Q000139:chemically induced* / Q000378:metabolism / Q000517:prevention & control; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*
D000970:Antineoplastic Agents; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D002945:Cisplatin