1. Ischemic acute tubular necrosis models and drug discovery: a focus on cellular inflammation.
- Author
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Ikeda M, Prachasilchai W, Burne-Taney MJ, Rabb H, and Yokota-Ikeda N
- Subjects
- Animals, Anti-Inflammatory Agents pharmacology, B-Lymphocytes drug effects, B-Lymphocytes metabolism, Cells, Cultured, Gene Expression Profiling, Gene Expression Regulation, Hydroxymethylglutaryl-CoA Reductase Inhibitors pharmacology, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Inflammation metabolism, Ischemia genetics, Ischemia metabolism, Kidney blood supply, Kidney Tubular Necrosis, Acute genetics, Kidney Tubular Necrosis, Acute metabolism, Mycophenolic Acid analogs & derivatives, Mycophenolic Acid pharmacology, Mycophenolic Acid therapeutic use, Oligonucleotide Array Sequence Analysis, T-Lymphocytes drug effects, T-Lymphocytes metabolism, Anti-Inflammatory Agents therapeutic use, Disease Models, Animal, Drug Evaluation, Preclinical methods, Inflammation drug therapy, Ischemia drug therapy, Kidney Tubular Necrosis, Acute drug therapy
- Abstract
Acute renal failure (ARF) is a common cause of mortality and morbidity in hospitalized patients. Ischemia is an important cause of ARF, and ARF caused by ischemic injury is referred to as ischemic acute tubular necrosis (ATN). There is growing evidence from models that ischemic ATN is associated with intrarenal inflammation. Consequently, intrarenal inflammation is an attractive target for the development of novel drug therapies for ARF. This review outlines ischemic ATN models, the pathophysiological roles of inflammatory cells such as T and B cells in ischemic ATN models, and effective T and B cell therapeutic reagents.
- Published
- 2006
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