Human Heme Oxygenase (HO)-1 Deficiency and the Oxidative Injury of Vascular Endothelial Cells
Heme oxygenase-1 (HO-1) constitutes one of the three isozymes of HO, which catalyze the degradation of heme into biliverdin, carbon monoxide (CO) and free iron.1, 2, 3, 4, 5 Recent experimental data indicate that one of the heme degradation products, CO acts on cellular metabolism to protect cells from oxidative stress and regulate production of inflammatory molecules.6, 7, 8 As a result, CO directly controls the inflammatory state of a given tissue and at the same time, regulates the level of microcirculation within the target organs acting as a gaseous vasodilator.9, 10, 11 Among three isozymes with similar enzyme activities, HO-1 is the only protein which is rapidly induced upon stimulation with various oxidative stresses.12, 13, 14 Therefore, it is suggested that any defect in its function will lead to uncontrollable inflammatory responses upon certain exogenous insults, such as infection and hemolysis.
KeywordsVascular Endothelial Cell Heme Oxygenase Oxidative Injury Endothelial Cell Injury Deletion Junction
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