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- W2029233458 endingPage "167" @default.
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- W2029233458 abstract "Heme oxygenases (HOs) are the rate-limiting enzymes in the catabolism of heme into biliverdin, free iron, and carbon monoxide. Two genetically distinct isoforms of HO have been characterized: an inducible form, HO-1, and a constitutively expressed form, HO-2. HO-1 is a kind of stress protein, and thus regarded as a sensitive and reliable indicator of cellular oxidative stress. The HO system acts as potent antioxidants, protects endothelial cells from apoptosis, is involved in regulating vascular tone, attenuates inflammatory response in the vessel wall, and participates in angiogenesis and vasculogenesis. Endothelial integrity and activity are thought to occupy the central position in the pathogenesis of cardiovascular diseases. Cardiovascular disease risk conditions converge in the contribution to oxidative stress. The oxidative stress leads to endothelial and vascular smooth muscle cell dysfunction with increases in vessel tone, cell growth, and gene expression that create a pro-thrombotic/pro-inflammatory environment. Subsequent formation, progression, and obstruction of atherosclerotic plaque may result in myocardial infarction, stroke, and cardiovascular death. This background provides the rationale for exploring the potential therapeutic role for HO system in the amelioration of vascular inflammation and prevention of adverse cardiovascular outcomes. Antioxid. Redox Signal. 14, 137–167. Introduction HO Expression Heme oxygenase-1 Mitogen-activated protein kinases Nrf2 and Bach1 Activator protein-1 Biliverdin reductase Heme oxygenase-2 HO By-Products Carbon monoxide Ferrous iron and ferritin BV and BR Effect of HO-1 on Vascular Inflammation Cytokines, chemokines, and mediators Macrophages Endothelial cells Control of Vascular Diseases by HO-1=CO Ischemic diseases Hypertension Atherosclerosis Diabetes mellitus Therapeutic potential of HO-1=CO in vascular diseases Effect of HO-1 on Angiogenesis Cross-talk between the HO-1=CO and NOS=NO pathways Effect of HO-1=CO pathway on vascular homeostasis Regulation of VEGF expression by HO-1=CO Restenosis and vasculopathy Conclusion" @default.
- W2029233458 created "2016-06-24" @default.
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- W2029233458 date "2011-01-01" @default.
- W2029233458 modified "2023-10-16" @default.
- W2029233458 title "Heme Oxygenase in the Regulation of Vascular Biology: From Molecular Mechanisms to Therapeutic Opportunities" @default.
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