Weidemann A, Bernhardt WM, Klanke B, Daniel C, Buchholz B, Campean V, Amann KU, Warnecke C, Wiesener MS, Eckardt KU, Willam C (2008)
Publication Status: Published
Publication Type: Journal article, Original article
Publication year: 2008
Publisher: AMER SOC NEPHROLOGY
Book Volume: 19
Pages Range: 486-494
Journal Issue: 3
The contribution of hypoxia to cisplatin-induced renal tubular injury is controversial. Because the hypoxia-inducible factor (HIF) pathway is a master regulator of adaptation to hypoxia, we measured the effects of cisplatin on HIF accumulation in vitro and in vivo, and tested whether hypoxic preconditioning is protective against cisplatin-induced injury. We found that cisplatin did not stabilize HIF-1 alpha protein in vitro or in vivo under normoxic conditions. However, hypoxic preconditioning of cisplatin-treated proximal tubular cells in culture reduced apoptosis in an HIF-1 alpha-dependent fashion and increased cell proliferation as measured by BrdU incorporation. In vivo, rats preconditioned with carbon monoxide before cisplatin administration had significantly better renal function than rats kept in normoxic conditions throughout. Moreover, the histomorphological extent of renal damage and tubular apoptosis was reduced by the preconditional treatment. Therefore, development of pharmacologic agents to induce renal HIF might provide a new approach to ameliorate cisplatin-induced nephrotoxicity.
APA:
Weidemann, A., Bernhardt, W.M., Klanke, B., Daniel, C., Buchholz, B., Campean, V.,... Willam, C. (2008). HIF activation protects from acute kidney injury. Journal of the American Society of Nephrology, 19(3), 486-494. https://doi.org/10.1681/ASN.2007040419
MLA:
Weidemann, Alexander, et al. "HIF activation protects from acute kidney injury." Journal of the American Society of Nephrology 19.3 (2008): 486-494.
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