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these results demonstrate that increased diaphragmatic levels of SOD2 are essential to achieve the full benefit of exercise-induced protection against VIDD.
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SOD2, which normally binds manganese, can incorporate iron and generate an alternative isoform with peroxidase activity.
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MnSOD deficiency exacerbated the mitochondrial rate of reactive oxygen species (ROS) production and myocardial oxidative stress in Chagas disease.
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Quiescence is initiated by the prion protein (PrP) and maintained through downstream increases in the expression and activity of superoxide dismutase-2 (SOD2) that reduces mitochondrial superoxide.
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Melatonin promoted MnSOD and SIRT1 expression, which successfully ameliorated busulfan-induced SSC apoptosis caused by high concentrations of ROS and p53
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deletion of intestinal SOD2 gene in mice results in increased susceptibility to colitis
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SOD2 expression is ATM- and RelA-dependent, ATM knockdown renders cells sensitive to pro-oxidant exposure, and SOD mimetics partially rescue this sensitivity. Mice with germline deletion of Atm fail to develop mature mammary glands, but using a conditional knockout approach, we determined that Atm deletion significantly diminished the expression of Sod2.
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Enhanced mitochondrial oxidative stress under hyperlipidemic conditions in aging induces plaque instability, in part by increasing smooth muscle cell apoptosis, necrotic core expansion, and matrix degradation in Sod2/ApoE knockout mice.
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Deletion of SOD2 increases mitochondrial reactive oxygen species but does not influence platelet function.
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This study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD.
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data showed that Klotho protects Tac-induced oxidative stress by negatively regulating the PI3K/AKT pathway and subsequently enhancing FoxO3a-mediated MnSOD expression.
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Moderate MnSOD and/or catalase overexpression in desmin-null hearts leads to a marked decrease in intracellular reactive oxygen species, ameliorates mitochondrial and other ultrastructural defects, minimizes myocardial degeneration and leads to a significant improvement of cardiac function.
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this study shows that differential protein acetylation assists import of excess SOD2 into mitochondria and mediates SOD2 aggregation associated with cardiac hypertrophy in the murine SOD2-tg heart
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SOD2 overexpression blocks maternal diabetes-induced oxidative stress and ER stress, and reduces the incidence of NTDs in embryos exposed to maternal diabetes
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the regulation of mitochondrial ROS by SOD2 and Sirt3 plays an important role in fine-tuning the Osteoclast differentiation program.
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treatment with Mito-TEMPO, a mitochondrial-specific superoxide scavenger, recovered mitochondrial fission-fusion imbalance and blunted mitochondrial superoxide production, and reduced the IDH2 knockdown-induced decrease in MnSOD expression, eNOS phosphorylation and NO production in endothelial cells
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On normal salt diet, renal CuZnSOD and ECSOD proteins were similar but renal MnSOD was lower in hGRK4g486V than Non-T mice and remained low on high salt diet. hGRK4gammawild-type mice were normotensive and hGRK4g142V mice were hypertensive but both were salt-resistant and in normal redox balance. Chronic tempol treatment partially prevented the salt-sensitivity of hGRK4g486V mice.
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when mice were challenged with chronic, peripheral infusion of AngII, only the MnSOD knock-down confined to the SFO, and not the periphery, demonstrated an increased sensitization and potentiated hypertension. In complementary experiments, over-expressing MnSOD in the SFO significantly decreased blood pressure in response to chronic AngII.
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results suggest that Sod2 is a target gene of LRH-1, and that LRH-1 agonists can mediate a reduction in ROS production and oxidative stress driven by an excess of fatty acids, as exhibited in nonalcoholic fatty liver disease
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We investigated the role of Mn-SOD in NIHL by examining the extent of hearing loss and hair cell damage after noise exposure in C57BL/6 wild-type (WT) mice and Mn-SOD heterozygous knockout (HET) mice. Mean ABR thresholds were significantly worse on post-noise exposure days 7 and 14 in HET mice compared with WT mice. Outer hair cell damage was significantly greater in all cochlear turns in HET mice compared with WT mice.
