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Our data suggest that Sod3 and extracellular oxidative stress may play an important role in the development of pneumoconiosis and pulmonary vascular remodeling following exposure to environmental and occupational silica.
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Akt2 plays a critical role in ATP7A protein stabilization and translocation to plasma membrane in vascular smooth muscle cells, which contributes to full activation of vascular SOD3 that protects against endothelial dysfunction in T2DM.
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Enhanced expression of EcSOD in skeletal muscle profoundly protects against multiple organ dysfunction syndrome by inhibiting endothelial activation and inflammatory cell adhesion.
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Epigenetic regulation of EC-SOD expression in aging lung fibroblasts is exerted via histone acetylation.
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Results indicate that medium molecular weight heparinyl phenylalanine (MHF) and medium molecular weight heparinyl leucine (MHL) show a radical scavenging ability by increasing the extracellular superoxide dismutase (EC-SOD) activity and MHF may be a candidate for clinical use.
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Thus, our findings suggest that deficient management of extracellular superoxide can lead to altered lung developmental signaling during alveogenesis in mice.
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the redistribution of SOD3 as a result of the R213G single-nucleotide polymorphism protects mice from bleomycin-induced fibrosis and secondary pulmonary hypertension by improved resolution of alveolar inflammation.
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These data reveal that ecSOD activity modulates neutrophil recruitment and function in a cell-extrinsic fashion, highlighting the importance of the enzyme in protecting tissues from oxidative damage.
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wound healing impairments in ageing are associated with increased levels of ROS, decreased SOD3 expression and impaired extracellular oxidative stress regulation
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FXR may regulate SOD3 expression to suppress reactive oxygen species production, resulting in decreasing JNK activity.
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Arginine 213 in the heparin-binding domain of SOD3 is critical for maintaining proper organ function through moderating the normal innate immune response, which would otherwise lead to chronic inflammation and degenerative diseases in aged mice.
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the rs1799895 polymorphism in extracellular superoxide dismutase affects cardiopulmonary disease risk by altering protein distribution
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the localized loss of pulmonary artery EC-SOD augments chronic hypoxic pulmonary hypertension. In addition to oxidative inactivation of nitric oxide, deletion of EC-SOD seems to reduce eNOS activity, further compromising pulmonary vascular function.
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Our results suggest that EC-SOD plays a dynamic role in the inflammatory response mounted by activated macrophages.
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reduced SOD3 expression correlates with alveolar injury measures in the recovered neonatal hyperoxic lung
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Data suggest that epigenetic silencing of EcSOD may contribute to mammary tumorigenesis and that restoring the extracellular superoxide scavenging activity could be an effective strategy for breast cancer treatment.
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When Cys195 was introduced, both active EC-SOD and a novel inactive EC-SOD were generated, and the specific activity of the EC-SOD was significantly reduced by the mutation.
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a decrease in ATP7A protein expression contributes to impaired SOD3 activity, resulting in O2(*-) overproduction and endothelial dysfunction in blood vessels of type 1 diabetes mellitus.
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Cardiac-selective expression of EcSOD from the cardiac troponin-T promoter after systemic administration of AAV9 provides significant protection against both acute myocardial infarction and left ventricular remodeling.
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EC-SOD plays a key role in preserving angiogenesis by scavenging free radicals which has an inhibitory effect on angiogenesis process in neonatal mice lung following exposure to hyperoxia.
