Heme Oxygenase-1/Carbon Monoxide
نویسندگان
چکیده
منابع مشابه
Heme oxygenase and hepatic microcirculation: more than just carbon monoxide?
(cGMP). Like NO , CO can also activate guanylate cyclase to cause vasodilation [5] ; however, previous studies have indicated that other mechanisms may contribute to the effects of CO on hepatic tone [6] . In their study [4] , the authors found some potentially novel mechanisms by which HO-1 mediates hepatic tone that appear independent of cGMP and, at least in part, independent of CO . The aut...
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Self-preservation is a fundamental tenet exhibited by all organisms and is perhaps most apparent when the organism is confronted by various threats to survival. This concept also holds true at the most basic cellular level where the cell coordinates a series of responses evolved to ensure the best chance of defense and survival. The ability of cells and tissues to mount an adaptive response to ...
متن کاملHeme oxygenase-1 and carbon monoxide suppress autoimmune neuroinflammation.
Heme oxygenase-1 (HO-1, encoded by HMOX1) dampens inflammatory reactions via the catabolism of heme into CO, Fe, and biliverdin. We report that expression of HO-1 dictates the pathologic outcome of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS). Induction of EAE in Hmox1(-/- )C57BL/6 mice led to enhanced CNS demyelination, paralysis, and mortality, as compar...
متن کاملHeme oxygenase-1 and carbon monoxide in pulmonary medicine
Heme oxygenase-1 (HO-1), an inducible stress protein, confers cytoprotection against oxidative stress in vitro and in vivo. In addition to its physiological role in heme degradation, HO-1 may influence a number of cellular processes, including growth, inflammation, and apoptosis. By virtue of anti-inflammatory effects, HO-1 limits tissue damage in response to proinflammatory stimuli and prevent...
متن کاملCytoprotection of heme oxygenase-1/carbon monoxide in lung injury.
Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) have been the major cause of morbidity and mortality in intensive care units (ICU) over the past decades despite advances in therapeutic modalities. This syndrome is characterized by noncardiogenic pulmonary edema, and pulmonary and systemic inflammation resulting in respiratory failure (1, 2). Both exudative and proliferati...
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ژورنال
عنوان ژورنال: American Journal of Respiratory Cell and Molecular Biology
سال: 2009
ISSN: 1044-1549,1535-4989
DOI: 10.1165/rcmb.2009-0170tr