scholarly journals Beneficial effects of the heme oxygenase-1/carbon monoxide system

Critical Care ◽  
2009 ◽  
Vol 13 (Suppl 1) ◽  
pp. P367
Author(s):  
N Takeyama ◽  
S Takaki ◽  
Y Kajita ◽  
T Yabuki ◽  
H Noguchi ◽  
...  
2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Myrna Constantin ◽  
Alexander J. S. Choi ◽  
Suzanne M. Cloonan ◽  
Stefan W. Ryter

Heme oxygenase (HO), a catabolic enzyme, provides the rate-limiting step in the oxidative breakdown of heme, to generate carbon monoxide (CO), iron, and biliverdin-IXα. Induction of the inducible form, HO-1, in tissues is generally regarded as a protective mechanism. Over the last decade, considerable progress has been made in defining the therapeutic potential of HO-1 in a number of preclinical models of lung tissue injury and disease. Likewise, tissue-protective effects of CO, when applied at low concentration, have been observed in many of these models. Recent studies have expanded this concept to include chemical CO-releasing molecules (CORMs). Collectively, salutary effects of the HO-1/CO system have been demonstrated in lung inflammation/acute lung injury, lung and vascular transplantation, sepsis, and pulmonary hypertension models. The beneficial effects of HO-1/CO are conveyed in part through the inhibition or modulation of inflammatory, apoptotic, and proliferative processes. Recent advances, however, suggest that the regulation of autophagy and the preservation of mitochondrial homeostasis may serve as additional candidate mechanisms. Further preclinical and clinical trials are needed to ascertain the therapeutic potential of HO-1/CO in human clinical disease.


2009 ◽  
Vol 36 (1) ◽  
pp. 42-48 ◽  
Author(s):  
Shoji Takaki ◽  
Naoshi Takeyama ◽  
Yuka Kajita ◽  
Teru Yabuki ◽  
Hiroki Noguchi ◽  
...  

2003 ◽  
Vol 4 (1) ◽  
Author(s):  
Dirk-Jan Slebos ◽  
Stefan W Ryter ◽  
Augustine MK Choi

2006 ◽  
Vol 290 (3) ◽  
pp. F563-F571 ◽  
Author(s):  
Kristin A. Kirkby ◽  
Christopher A. Adin

Heme oxygenase 1 (HO-1) is induced in response to cellular stress and is responsible for converting the prooxidant heme molecule into equimolar quantities of biliverdin (BV), carbon monoxide (CO), and iron. BV is then converted to bilirubin (BR) by the enzyme biliverdin reductase. Experimental evidence suggests that induction of the HO system is an important endogenous mechanism for cytoprotection and that the downstream products of heme degradation, CO, BR, and BV, may mediate these powerful beneficial effects. These molecules, which were once considered to be toxic metabolic waste products, have recently been shown to have dose-dependent vasodilatory, antioxidant, and anti-inflammatory properties that are particularly desirable for tissue protection during organ transplantation. In fact, recent work has demonstrated that administration of exogenous CO, BR, or BV may offer a simple, inexpensive method to substitute for the cytoprotective effects of HO-1 in a variety of clinically applicable models. This review will attempt to summarize the relevant biochemical and cytoprotective properties of CO, BR, and BV, and will discuss emerging studies involving the therapeutic applications of these molecules in the kidney and other organ systems.


2007 ◽  
Vol 21 (13) ◽  
pp. 3450-3457 ◽  
Author(s):  
Soo Sun Lee ◽  
Wenda Gao ◽  
Silvia Mazzola ◽  
Michael N. Thomas ◽  
Eva Csizmadia ◽  
...  

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