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See related article, pages 919–927 Heme oxygenase (HO)-1 catalyzes the rate-limiting step in the metabolic conversion of heme to bilirubin, iron, and carbon monoxide (CO).1 Ample literature has demonstrated that exogenous or endogenously-produced CO possesses signaling properties affecting numerous critical cellular processes including inflammation, cellular proliferation, and apoptotic cell death.1,2 CO and the bile pigments biliverdin and bilirubin play important physiological roles in the circulation. The production of CO in vascular cells modulates blood flow and blood fluidity by regulating vasomotor tone and inhibiting smooth muscle cell proliferation and platelet aggregation. CO also maintains vessel wall integrity by directly blocking apoptosis and inhibiting the release of proinflammatory cytokines from the vessel wall. These effects of CO are mediated via multiple pathways, including activation of soluble guanylate cyclase, p38 mitogen-activated protein kinase (MAPK), and potassium channels.1,2 Induction of HO-1 gene expression and the subsequent release of CO and bile pigments are observed in numerous vascular disorders providing an adaptive response to preserve homeostasis at sites of vascular injury. Hence, the formation of CO and bile pigments in vascular cells may function as an important vasoprotective system.1,2Thus far, several transcriptional factors (TF) have been implicated in HO-1 gene expression. Among these TFs, the heat-shock, nuclear factor-κB (NF-κB), nuclear factor–erythroid 2-related factor 2 (Nrf2), and activator protein–1 families are the most important regulators of cellular stress responses. Nrf2 is activated by various xenobiotics and oxidants and regulates genes encoding proteins …

A New Road to Induce Heme Oxygenase-1 Expression by Carbon Monoxide