A common clinical condition, acute kidney injury (AKI) significantly influences morbidity and mortality, particularly in critically ill patients. The pathophysiology of AKI is complex and involves multiple pathways, including inflammation, autophagy, cell-cycle progression, and oxidative stress. Recent evidence suggests that a single insult to the kidney significantly enhances the propensity to develop chronic kidney disease. Therefore, the generation of effective therapies against AKI is timely. In this context, the cytoprotective effects of heme oxygenase 1 (HO-1) in animal models of AKI are well documented. HO-1 modulates oxidative stress, autophagy, and inflammation and regulates the progression of cell cycle via direct and indirect mechanisms. These beneficial effects of HO-1 induction during AKI are mediated in part by the by-products of the HO reaction (iron, carbon monoxide, and bile pigments). This review highlights recent advances in the molecular mechanisms of HO-1-mediated cytoprotection and discusses the translational potential of HO-1 induction in AKI.
Keywords: Acute kidney injury (AKI); HMOX1; autophagic response; biomarker; cell cycle regulation; cytoprotection; heme oxygenase 1 (HO-1); inflammation; oxidative stress; pathophysiology; renal failure; review; translational research.
Copyright © 2016 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.