Cardiomyocyte-restricted overexpression of extracellular superoxide dismutase increases nitric oxide bioavailability and reduces infarct size after ischemia/reperfusion
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Summary
These findings are the first to demonstrate increased NO bioavailability with attenuation of ROS by direct measurement of these reactive species (EPR, reactive fluorescent dyes with cardiac-specific ecSOD expression) and the first indication that the predominantly extracellular SOD isoform is capable of cytosolic localization that affects myocardial intracellular signal transduction and function.
- Type
- article
- Published
- 2012-10-26
- Cited by
- 50
- References
- 72
- Access
- Open access
- OpenAlex
- https://openalex.org/W23099819
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:15327149
Keywords
Product (mathematics), Nuclear fission product, Computer science, Chemistry, Fission products
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- Mitochondrial Dynamics: Exploring A Novel Target Against Myocardial Ischemia-Reperfusion Injury
- Ischemia-Reperfusion Injury in Stroke
- Exercise-induced cardioprotection: a role for eNOS uncoupling and NO metabolites
- Deficiency of Ataxia Telangiectasia Mutated Kinase Modulates Cardiac Remodeling Following Myocardial Infarction: Involvement in Fibrosis and Apoptosis
- Kinetic and mechanistic considerations to assess the biological fate of peroxynitrite
- Characterization of oxygen radical formation mechanism at early cardiac ischemia
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- Reoxygenation‐Derived Toxic Reactive Oxygen/Nitrogen Species Modulate the Contribution of Bone Marrow Progenitor Cells to Remodeling After Myocardial Infarction
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- Loss of Mrp1 Potentiates Doxorubicin-Induced Cytotoxicity in Neonatal Mouse Cardiomyocytes and Cardiac Fibroblasts.