ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Protective effect of extracellular superoxide dismutase on endothelial function during aging.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- Sex-Dependent Impairment of Endothelium-Dependent Relaxation in Aorta of Mice with Overexpression of Hyaluronan in Tunica Media.International journal of molecular sciences · 2023Article
- Pharmacological Activation of Nrf2 by Rosolic Acid Attenuates Endoplasmic Reticulum Stress in Endothelial Cells.Oxidative medicine and cellular longevity · 2021Article
- Caveolin-1 stabilizes ATP7A, a copper transporter for extracellular SOD, in vascular tissue to maintain endothelial function.American journal of physiology. Cell physiology · 2020Article
- Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise.Redox biology · 2020Review
- Carotid Disease and Ageing: A Literature Review on the Pathogenesis of Vascular Senescence in Older Subjects.Current gerontology and geriatrics research · 2020Review
- Role of endothelial NADAmerican journal of physiology. Heart and circulatory physiology · 2019Review
- Is cellular senescence involved in cystic fibrosis?Respiratory research · 2019Review
- Akt2 (Protein Kinase B Beta) Stabilizes ATP7A, a Copper Transporter for Extracellular Superoxide Dismutase, in Vascular Smooth Muscle: Novel Mechanism to Limit Endothelial Dysfunction in Type 2 Diabetes Mellitus.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Proinflammatory Arterial Stiffness Syndrome: A Signature of Large Arterial Aging.Journal of vascular research · 2018Review
- Muscle-derived extracellular superoxide dismutase inhibits endothelial activation and protects against multiple organ dysfunction syndrome in mice.Free radical biology & medicine · 2017Article
- Mitochondrial function in hypoxic ischemic injury and influence of aging.Progress in neurobiology · 2017Review
- Genomic and phenotypic signatures of climate adaptation in anEcology and evolution · 2017Article
- Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries.Journal of molecular and cellular cardiology · 2015Review
- Mechanisms of superoxide signaling in epigenetic processes: relation to aging and cancer.Aging and disease · 2015Review
- Aortic valve sclerosis in mice deficient in endothelial nitric oxide synthase.American journal of physiology. Heart and circulatory physiology · 2014Article
- The use of the Cre/loxP system to study oxidative stress in tissue-specific manganese superoxide dismutase knockout models.Antioxidants & redox signaling · 2014Review
- The role of oxidative stress and inflammation in cardiovascular aging.BioMed research international · 2014Review
- Transcriptional and phenotypic changes in aorta and aortic valve with aging and MnSOD deficiency in mice.American journal of physiology. Heart and circulatory physiology · 2013Article
- Interleukin-10 protects against aging-induced endothelial dysfunction.Physiological reports · 2013Article
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Abstract
Endothelial vasomotor function decreases with increasing age. Extracellular superoxide dismutase (ecSOD) protects against vascular dysfunction in several disease states. The purpose of this study was to determine whether endogenous ecSOD protects against endothelial dysfunction in old mice. Vasomotor function of the aorta was studied ex vivo in wild-type (ecSOD(+/+)) and ecSOD-deficient (ecSOD(-/-)) mice at 11 (adult) and 29 (old) mo of age. Maximal relaxation to acetylcholine (10(-4) M) was impaired in vessels from adult ecSOD(-/-) mice [75 +/- 3% (mean +/- SE)] compared with wild-type mice (89 +/- 2%, P < 0.05). Maximal relaxation to acetylcholine (10(-4) M) was profoundly impaired in aorta from old ecSOD(-/-) mice (45 +/- 5%) compared with wild-type mice (75 +/- 4%, P < 0.05). There was a significant correlation between expression of ecSOD and maximal relaxation to acetylcholine in adult and old mice. Tempol (1 mM), a scavenger of superoxide, improved relaxation in response to acetylcholine (63 +/- 8%) in old ecSOD(-/-) mice (P < 0.05), but not wild-type mice (75 +/- 4%). Maximal relaxation to sodium nitroprusside was similar in aorta from adult and old wild-type and ecSOD(-/-) mice. Quantitative RT-PCR showed a decrease in mRNA levels of ecSOD and catalase in aorta of old mice and an increase in levels of TNFalpha and Nox-4 in aorta of old mice compared with adult mice. The findings support the hypothesis that impaired antioxidant mechanisms may contribute to cumulative increases in oxidative stress and impaired endothelial function in old mice. In conclusion, endogenous ecSOD plays an important role in protection against endothelial dysfunction during aging.
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