The story so far: Molecular regulation of the heme oxygenase-1 gene in renal injury

Eric M. Sikorski, Thomas Hock, Nathalie Hill-Kapturczak, Anupam Agarwal

Research output: Contribution to journalReview articlepeer-review

194 Scopus citations

Abstract

Heme oxygenases (HOs) catalyze the rate-limiting step in heme degradation, resulting in the formation of iron, carbon monoxide, and biliverdin, the latter of which is subsequently converted to bilirubin by biliverdin reductase. Recent attention has focused on the biological effects of product(s) of this enzymatic reaction, which have important antioxidant, anti-inflammatory, and cytoprotective functions. Two major isoforms of the HO enzyme have been described: an inducible isoform, HO-1, and a constitutively expressed isoform, HO-2. A third isoform, HO-3, closely related to HO-2, has also been described. Several stimuli implicated in the pathogenesis of renal injury, such as heme, nitric oxide, growth factors, angiotensin II, cytokines, and nephrotoxins, induce HO-1. Induction of HO-1 occurs as an adaptive and beneficial response to these stimuli, as demonstrated by studies in renal and non-renal disease states. This review will focus on the molecular regulation of the HO-1 gene in renal injury and will highlight the interspecies differences, predominantly between the rodent and human HO-1 genes.

Original languageEnglish (US)
Pages (from-to)F425-F441
JournalAmerican Journal of Physiology - Renal Physiology
Volume286
Issue number3 55-3
DOIs
StatePublished - Mar 2004

Keywords

  • Gene transcription
  • Heme proteins
  • Oxidant stress

ASJC Scopus subject areas

  • Physiology
  • Urology

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