Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/20108
Title: Targeting HIF-1α to Prevent Renal Ischemia-Reperfusion Injury: Does It Work?
Authors: Sethi, Kapil;Rao, Kenny;Bolton, Damien M;Patel, Oneel;Ischia, Joseph J
Affiliation: Department of Surgery, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Department of Urology, Austin Health, Heidelberg, Victoria, Australia
Issue Date: 25-Nov-2018
EDate: 2018-11-25
Citation: International journal of cell biology 2018; 2018: 9852791
Abstract: Partial nephrectomy (open or minimally invasive) usually requires temporary renal arterial occlusion to limit intraoperative bleeding and improve access to intrarenal structures. This is a time-critical step due to the critical ischemia period of renal tissue. Prolonged renal ischemia may lead to irreversible nephron damage in the remaining tissue and, ultimately, chronic kidney disease. This is potentiated by the incompletely understood ischemia-reperfusion injury (IRI). A key mechanism in IRI prevention appears to be the upregulation of an intracellular transcription protein, Hypoxia-Inducible Factor (HIF). HIF mediates metabolic adaptation, angiogenesis, erythropoiesis, cell growth, survival, and apoptosis. Upregulating HIF-1α via ischemic preconditioning (IPC) or drugs that simulate hypoxia (hypoxia-mimetics) has been investigated as a method to reduce IRI. While many promising chemical agents have been trialed for the prevention of IRI in small animal studies, all have failed in human trials. The aim of this review is to highlight the techniques and drugs that target HIF-1α and ameliorate IRI associated with renal ischemia. Developing a technique or drug that could reduce the risk of acute kidney injury associated with renal IRI would have an immediate worldwide impact on multisystem surgeries that would otherwise risk ischemic tissue injury.
URI: http://ahro.austin.org.au/austinjspui/handle/1/20108
DOI: 10.1155/2018/9852791
ORCID: 0000-0002-6037-8895
0000-0002-5145-6783
PubMed URL: 30595695
ISSN: 1687-8876
Type: Journal Article
Review
Appears in Collections:Journal articles

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