This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Choi, A. M.K. Search for Related Content PubMed PubMed Citation Articles by Choi, A. M.K. Pubmed/NCBI databases Medline Plus Health Information Cardiomyopathy

(Circulation Research. 2001;89:105.)
© 2001 American Heart Association, Inc.

Editorial

Heme Oxygenase-1 Protects the Heart

Augustine M.K. Choi

From the Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pa.

Correspondence to Augustine M.K. Choi, MD, Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, MUH 628 NW, Pittsburgh, PA 15213. E-mail choiam@msx.upmc.edu

Key Words: carbon monoxide • bilirubin • ferritin

The seminal discovery of nitric oxide (NO) in the 1980s unraveled the novel concept that an endogenous production of a gaseous substance such as NO can impart diverse and critical functional effects on a wide spectrum of biological and pathological processes. Intense investigations in the chemistry and biology of NO have led to numerous fruitful discoveries, enhancing our understanding of many disease processes including cardiovascular disorders. Interestingly, though, we have known for a longer period of time that there exists another gaseous molecule, carbon monoxide (CO), which can be generated endogenously. The heme oxygenase (HO) enzyme system generates the majority of endogenous CO.^1,2 Since the biochemical isolation of the HO enzyme in 1968, much of the focus of HO research has been in the study of HO in heme metabolism based on the known fact that the HO enzyme serves as the rate-limiting enzyme in the degradation of heme. However, in recent years, as a result of the emerging role of HO in a variety of biological processes, interest in HO has continued to grow beyond its role in heme metabolism and has expanded into many scientific disciplines. The recent characterization of the HO enzyme system in yeast, prokaryotic bacterial system, and plants further highlights the functional importance of a highly conserved enzyme throughout the evolution of living organisms.

HO catalyzes the first and rate-limiting step in the degradation of heme to yield equimolar quantities of biliverdin IXa, CO, and iron^1,2 (Figure). Biliverdin is subsequently converted to bilirubin . . . [Full Text of this Article]

This article has been cited by other articles:

				Q. Li, Y. Guo, Q. Ou, C. Cui, W.-J. Wu, W. Tan, X. Zhu, L. B. Lanceta, S. K. Sanganalmath, B. Dawn, et al. Gene Transfer of Inducible Nitric Oxide Synthase Affords Cardioprotection by Upregulating Heme Oxygenase-1 Via a Nuclear Factor-{kappa}B-Dependent Pathway Circulation, September 29, 2009; 120(13): 1222 - 1230. [Abstract] [Full Text] [PDF]

				N. K. Idriss, A. D. Blann, and G. Y.H. Lip Hemoxygenase-1 in Cardiovascular Disease J. Am. Coll. Cardiol., September 16, 2008; 52(12): 971 - 978. [Abstract] [Full Text] [PDF]

				Y. L. Tang, Y. Tang, Y. C. Zhang, K. Qian, L. Shen, and M. I. Phillips Improved Graft Mesenchymal Stem Cell Survival in Ischemic Heart With a Hypoxia-Regulated Heme Oxygenase-1 Vector J. Am. Coll. Cardiol., October 4, 2005; 46(7): 1339 - 1350. [Abstract] [Full Text] [PDF]

				S. F. Ameriso, A. R. Villamil, C. Zedda, J. C. Parodi, S. Garrido, M. I. Sarchi, M. Schultz, J. Boczkowski, and G. E. Sevlever Heme Oxygenase-1 Is Expressed in Carotid Atherosclerotic Plaques Infected by Helicobacter pylori and Is More Prevalent in Asymptomatic Subjects Stroke, September 1, 2005; 36(9): 1896 - 1900. [Abstract] [Full Text] [PDF]

				J. Tongers, B. Fiedler, D. Konig, T. Kempf, G. Klein, J. Heineke, T. Kraft, S. Gambaryan, S. M Lohmann, H. Drexler, et al. Heme oxygenase-1 inhibition of MAP kinases, calcineurin/NFAT signaling, and hypertrophy in cardiac myocytes Cardiovasc Res, August 15, 2004; 63(3): 545 - 552. [Abstract] [Full Text] [PDF]

				M. de Perrot, M. Liu, T. K. Waddell, and S. Keshavjee Ischemia-Reperfusion-induced Lung Injury Am. J. Respir. Crit. Care Med., February 15, 2003; 167(4): 490 - 511. [Abstract] [Full Text] [PDF]

				N. Bodyak, P. M. Kang, M. Hiromura, I. Sulijoadikusumo, N. Horikoshi, K. Khrapko, and A. Usheva Gene expression profiling of the aging mouse cardiac myocytes Nucleic Acids Res., September 1, 2002; 30(17): 3788 - 3794. [Abstract] [Full Text] [PDF]