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| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C1801960 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C0001985 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C1444749 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C0024708 | lld:lifeskim |
| pubmed-article:18596060 | lifeskim:mentions | umls-concept:C0436331 | lld:lifeskim |
| pubmed-article:18596060 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:18596060 | pubmed:dateCreated | 2008-10-16 | lld:pubmed |
| pubmed-article:18596060 | pubmed:abstractText | Imbalance between pro- and antioxidant species (e.g. during aging) plays a crucial role for vascular function and is associated with oxidative gene regulation and modification. Vascular aging is associated with progressive deterioration of vascular homeostasis leading to reduced relaxation, hypertrophy, and a higher risk of thrombotic events. These effects can be explained by a reduction in free bioavailable nitric oxide that is inactivated by an age-dependent increase in superoxide formation. In the present study, mitochondria as a source of reactive oxygen species (ROS) and the contribution of manganese superoxide dismutase (MnSOD, SOD-2) and aldehyde dehydrogenase (ALDH-2) were investigated. | lld:pubmed |
| pubmed-article:18596060 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18596060 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18596060 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18596060 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18596060 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18596060 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18596060 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:18596060 | pubmed:issn | 0008-6363 | lld:pubmed |
| pubmed-article:18596060 | pubmed:author | pubmed-author:KawamotoToshi... | lld:pubmed |
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| pubmed-article:18596060 | pubmed:author | pubmed-author:MünzelThomasT | lld:pubmed |
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| pubmed-article:18596060 | pubmed:volume | 80 | lld:pubmed |
| pubmed-article:18596060 | pubmed:owner | NLM | lld:pubmed |
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| pubmed-article:18596060 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18596060 | pubmed:articleTitle | Manganese superoxide dismutase and aldehyde dehydrogenase deficiency increase mitochondrial oxidative stress and aggravate age-dependent vascular dysfunction. | lld:pubmed |
| pubmed-article:18596060 | pubmed:affiliation | Second Medical Clinic, Department of Cardiology, Johannes Gutenberg University, Mainz, Germany. | lld:pubmed |
| pubmed-article:18596060 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18596060 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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