Acute kidney injury (AKI) is attended by injury-related biomarkers appearing in the urine and serum, decreased urine output, and impaired glomerular filtration rate. AKI causes increased morbidity and mortality and can progress to chronic kidney disease and end-stage kidney failure. AKI is without specific therapies and is managed by supported care. Heme oxygenase-1 (HO-1) is a cytoprotective, inducible enzyme that degrades toxic free heme released from destabilized heme proteins and, during this process, releases beneficial by-products such as carbon monoxide and biliverdin/bilirubin and promotes ferritin synthesis. HO-1 induction protects against assorted renal insults as demonstrated by in vitro and preclinical models. This review summarizes the advances in understanding of the protection conferred by HO-1 in AKI, how HO-1 can be induced including via its transcription factor Nrf2, and HO-1 induction as a therapeutic strategy.

Acute kidney injury (AKI) is attended by injury-related biomarkers appearing in the urine and serum, decreased urine output, and impaired glomerular filtration rate. AKI causes increased morbidity and mortality and can progress to chronic kidney disease and end-stage kidney failure. AKI is without specific therapies and is managed by supported care. Heme oxygenase-1 (HO-1) is a cytoprotective, inducible enzyme that degrades toxic free heme released from destabilized heme proteins and, during this process, releases beneficial by-products such as carbon monoxide and biliverdin/bilirubin and promotes ferritin synthesis. HO-1 induction protects against assorted renal insults as demonstrated by in vitro and preclinical models. This review summarizes the advances in understanding of the protection conferred by HO-1 in AKI, how HO-1 can be induced including via its transcription factor Nrf2, and HO-1 induction as a therapeutic strategy.