Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Antioxidants improve the phenotypes of dilated cardiomyopathy and muscle fatigue in mitochondrial superoxide dismutase-deficient mice.

Molecules (Basel, Switzerland) - 24 Jan 2013

Koyama Hirofumi, Nojiri Hidetoshi, Kawakami Satoru, Sunagawa Tadahiro, Shirasawa Takuji, Shimizu Takahiko

Abstract excerpt

Redox imbalance elevates the reactive oxygen species (ROS) level in cells and promotes age-related diseases. Superoxide dismutases (SODs) are antioxidative enzymes that catalyze the degradation of ROS. There are three SOD isoforms: SOD1/CuZn-SOD, SOD2/Mn-SOD, and SOD3/EC-SOD. SOD2, which is localized in the mitochondria, is an essential enzyme required for mouse survival, and systemic knockout causes neonatal...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antioxidants
Share to Cardiomyopathy, Dilated

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to SOD1 gene

Share to SOD2 gene

Share to Mitochondria

Share to Phenotype

Share to Superoxide Dismutase

Source

Open in PubMed Open full text

Identifiers

PMID: 23348992
DOI: 10.3390/molecules18021383
PMCID: PMC6269947

Genes

SOD2
SOD1
SOD3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Antioxidants improve the phenotypes of dilated cardiomyopathy and muscle fatigue in mitochondrial superoxide dismutase-deficient mice.PMID 23348992Read ↗

Mitochondrial superoxide radicals differentially affect muscle activity and neural function.Semantic proximity Read ↗

SOD2 in Skeletal Muscle: New Insights from an Inducible Deletion ModelSemantic proximity Read ↗

Heterozygous deficiency of manganese superoxide dismutase results in severe lipid peroxidation and spontaneous apoptosis in murine myocardium in vivo.Semantic proximity Read ↗

Genetic modification of prenatal lethality and dilated cardiomyopathy in Mn superoxide dismutase mutant mice.Semantic proximity Read ↗

Pathological Relationship between Intracellular Superoxide Metabolism and p53 Signaling in Mice.Semantic proximity Read ↗

Inducible and reversible SOD2 knockdown in mouse skeletal muscle drives impaired pyruvate oxidation and reduced metabolic flexibilitySemantic proximity Read ↗

Mitochondrial reactive oxygen species in mice lacking superoxide dismutase 2: attenuation via antioxidant treatment.Semantic proximity Read ↗

Conditional knockout of Mn-SOD targeted to type IIB skeletal muscle fibers increases oxidative stress and is sufficient to alter aerobic exercise capacity.Semantic proximity Read ↗

Skeletal muscle is a primary target of SOD1G93A-mediated toxicity.Semantic proximity Read ↗

Different extent of cardiac malfunction and resistance to oxidative stress in heterozygous and homozygous manganese-dependent superoxide dismutase-mutant mice.Semantic proximity Read ↗

A correlation of reactive oxygen species accumulation by depletion of superoxide dismutases with age-dependent impairment in the nervous system and muscles of Drosophila adults.Semantic proximity Read ↗

Heart-Specific Knockout of the Mitochondrial Thioredoxin Reductase (Txnrd2) Induces Metabolic and Contractile Dysfunction in the Aging Myocardium.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.