The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Preconditional Activation of Hypoxia-Inducible Factors Ameliorates Ischemic Acute Renal Failure
Abstract
Activation of hypoxia-inducible transcription factor (HIF) has been identified as an important mechanism of cellular adaptation to low oxygen. Normoxic degradation of HIF is mediated by oxygen-dependent hydroxylation of specific prolyl residues of the regulative alpha-subunits by HIF prolyl hydroxylases (PHD). It was hypothesized that inhibition of HIF degradation by either hypoxia or pharmacologic inhibition of PHD would confer protection against subsequent ischemic injury. For testing this hypothesis ischemic acute renal failure was induced in rats by 40 min of clamping of the left renal artery after right-sided nephrectomy. Before surgery, pretreatment with either carbon monoxide, leading to tissue hypoxia, or the novel PHD inhibitor FG-4487 was applied. No toxic effects of FG-4487 were observed. Both pretreatments strongly induced the accumulation of HIF-1alpha and HIF-2alpha in tubular and peritubular cells, respectively, as well as HIF target gene expression. The course of subsequent ischemic injury was significantly ameliorated by both strategies of preconditioning, as evident from a significant improvement of serum creatinine and serum urea after 24 and 72 h. Furthermore, tissue injury and apoptosis were less severe, which were quantified by application of a standardized histologic scoring system in a blinded manner. In conclusion, the data provide proof of principle that preconditional activation of the HIF system protects against ischemic injury. Inhibiting the activity of HIF hydroxylases therefore seems to have considerable clinical perspectives.
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Citations
Cites
Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.
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A conserved family of prolyl-4-hydroxylases that modify HIF
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Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway
Otterbein, L. E., Bach, F. H., Alam, J., Soares, M., Tao Lu, H., Wysk, M., Davis, R. J., Flavell, R. A., & Choi, A. M. K. (2000) · Nature Medicine · doi:10.1038/74680 · Cited by 2,153
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Oxygen sensing by HIF hydroxylases
Schofield, C. J., & Ratcliffe, P. J. (2004) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1366 · Cited by 2,068 · cited 1×
“To mark HIF- for degradation, specific prolyl residues are hydroxylated by an enzyme family of HIF-prolyl hydroxylases (prolyl hydroxylation domain protein [PHD]), which require dioxygen and 2-oxoglutarate as co-substrates (reviewed in ref [5]).”
BackgroundHIF-1α is essential for myeloid cell-mediated inflammation
Cramer, T., Yamanishi, Y., Clausen, B. E., Förster, I., Pawlinski, R., Mackman, N., Haase, V. H., Jaenisch, R., Corr, M., Nizet, V., et al. (2003) · Cell · doi:10.1016/s0092-8674(03)00154-5 · Cited by 2,046
Hypoxia of the Renal Medulla — Its Implications for Disease
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Widespread, hypoxia‐inducible expression of HIF‐2α in distinct cell populations of different organs
Wiesener, M. S., Jürgensen, J. S., Rosenberger, C., Scholze, C., Hörstrup, J. H., Warnecke, C., Mandriota, S., Bechmann, I., Frei, U. A., Pugh, C. W., et al. (2003) · The FASEB Journal · doi:10.1096/fj.02-0445fje · Cited by 740
Self-citationExpression of Hypoxia-Inducible Factor-1α and -2α in Hypoxic and Ischemic Rat Kidneys
Rosenberger, C., Mandriota, S., Ju[Combining Diaeresis]rgensen, J. S., Wiesener, M. S., Ho[Combining Diaeresis]rstrup, J. H., Frei, U., Ratcliffe, P. J., Maxwell, P. H., Bachmann, S., & Eckardt, K.-U. (2002) · Journal of the American Society of Nephrology · doi:10.1097/01.asn.0000017223.49823.2a · Cited by 567
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Cited by
Oxygen sensing by metazoans: the central role of the HIF hydroxylase pathway.
Kaelin, W. G., & Ratcliffe, P. J. (2008) · Molecular Cell · doi:10.1016/j.molcel.2008.04.009 · Cited by 3,251
Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition
Higgins, D. F., Kimura, K., Bernhardt, W. M., Shrimanker, N., Akai, Y., Hohenstein, B., Saito, Y., Johnson, R. S., Kretzler, M., Cohen, C. D., et al. (2007) · Journal of Clinical Investigation · doi:10.1172/jci30487 · Cited by 976
Self-citationHIF-1α-BNIP3-mediated mitophagy in tubular cells protects against renal ischemia/reperfusion injury
Fu, Z.-J., Wang, Z.-Y., Xu, L., Chen, X.-H., Li, X.-X., Liao, W.-T., Ma, H.-K., Jiang, M.-D., Xu, T.-T., Xu, J., et al. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101671 · Cited by 382
Interdependent roles for hypoxia inducible factor and nuclear factor‐κB in hypoxic inflammation
Taylor, C. T. (2008) · The Journal of Physiology · doi:10.1113/jphysiol.2008.157669 · Cited by 354
Inhibition of Prolyl Hydroxylases Increases Erythropoietin Production in ESRD
Bernhardt, W. M., Wiesener, M. S., Scigalla, P., Chou, J., Schmieder, R. E., Günzler, V., & Eckardt, K.-U. (2010) · Journal of the American Society of Nephrology · doi:10.1681/asn.2010010116 · Cited by 340
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Metadata
- Authors
- Bernhardt, W. M., Ca[Combining Circumflex Accent]mpean, V., Kany, S., Ju[Combining Diaeresis]rgensen, J.-S., Weidemann, A., Warnecke, C., Arend, M., Klaus, S., Gu[Combining Diaeresis]nzler, V., Amann, K., Willam, C., Wiesener, M. S., & Eckardt, K.-U.
- Venue
- Journal of the American Society of Nephrology
- Published
- 2006-07
- Volume
- 17
- Issue
- 7
- Pages
- 1970-1978
- ISSN
- 1046-6673 (ISSN-L)
- OpenAlex
- W2136548506
- Cited by
- 295
- References
- 32
- FWCI
- 15.13
- Type
- journal article
- Language
- en
- Open access
- closed
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- Bernhardt, W. M., Ca[Combining Circumflex Accent]mpean, V., Kany, S., Ju[Combining Diaeresis]rgensen, J.-S., Weidemann, A., Warnecke, C., Arend, M., Klaus, S., Gu[Combining Diaeresis]nzler, V., Amann, K., Willam, C., Wiesener, M. S., & Eckardt, K.-U. (2006). Preconditional Activation of Hypoxia-Inducible Factors Ameliorates Ischemic Acute Renal Failure. Journal of the American Society of Nephrology. https://doi.org/10.1681/asn.2005121302
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