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(Circulation Research. 2007;101:862.)
© 2007 American Heart Association, Inc.

Editorials

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

Hong Pyo Kim, Augustine M.K. Choi

From the Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pa. A.M.K.C. is currently at the Lung Biology Center, Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital, Boston, Mass.

Correspondence to Dr Choi, Lung Biology Center, Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115. E-mail amchoi@rics.bwh.harvard.edu

See related article, pages 919–927

Key Words: carbon monoxide • heme oxygenase-1 • PERK • Nrf-2 • anti-apoptosis • autophagy

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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.^1,2

Thus far, several transcriptional factors (TF) have been implicated in HO-1 gene expression. Among these TFs, the heat-shock, nuclear factor-B (NF-B), 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 with antioxidant and xenobiotic detoxification activities.³ Besides exogenous stimuli, physiological effectors such as hormones and . . . [Full Text of this Article]

Related Article:

Carbon Monoxide Induces Heme Oxygenase-1 via Activation of Protein Kinase R–Like Endoplasmic Reticulum Kinase and Inhibits Endothelial Cell Apoptosis Triggered by Endoplasmic Reticulum Stress

Ki Mo Kim, Hyun-Ock Pae, Min Zheng, Raekil Park, Young-Myeong Kim, and Hun-Taeg Chung
Circ. Res. 2007 101: 919-927. [Abstract] [Full Text] [PDF]

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