Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation
Although the exact mechanism through which NADPH oxidases (Nox’s) generate reactive oxygen species (ROS) is still not completely understood, it is widely considered that ROS accumulation is the cause of oxidative stress in endothelial cells. Increasing pieces of evidence strongly indicate the role f...
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | International Journal of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2012/678190 |
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| author | Nhat-Tu Le James P. Corsetti Janet L. Dehoff-Sparks Charles E. Sparks Keigi Fujiwara Jun-ichi Abe |
| author_facet | Nhat-Tu Le James P. Corsetti Janet L. Dehoff-Sparks Charles E. Sparks Keigi Fujiwara Jun-ichi Abe |
| author_sort | Nhat-Tu Le |
| collection | DOAJ |
| description | Although the exact mechanism through which NADPH oxidases (Nox’s) generate reactive oxygen species (ROS) is still not completely understood, it is widely considered that ROS accumulation is the cause of oxidative stress in endothelial cells. Increasing pieces of evidence strongly indicate the role for ROS in endothelial inflammation and dysfunction and subsequent development of atherosclerotic plaques, which are causes of various pathological cardiac events. An overview for a causative relationship between ROS and endothelial inflammation will be provided in this review. Particularly, a crucial role for specific protein SUMOylation in endothelial inflammation will be presented. Given that SUMOylation of specific proteins leads to increased endothelial inflammation, targeting specific SUMOylated proteins may be an elegant, effective strategy to control inflammation. In addition, the involvement of ROS production in increasing the risk of recurrent coronary events in a sub-group of non-diabetic, post-infarction patients with elevated levels of HDL-cholesterol will be presented with the emphasis that elevated HDL-cholesterol under certain inflammatory conditions can lead to increased incidence of cardiovascular events. |
| format | Article |
| id | doaj-art-ca2f49d853cc4233a0382c6672865b48 |
| institution | Kabale University |
| issn | 2090-8040 2042-0099 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Inflammation |
| spelling | doaj-art-ca2f49d853cc4233a0382c6672865b482025-02-03T01:01:14ZengWileyInternational Journal of Inflammation2090-80402042-00992012-01-01201210.1155/2012/678190678190Reactive Oxygen Species, SUMOylation, and Endothelial InflammationNhat-Tu Le0James P. Corsetti1Janet L. Dehoff-Sparks2Charles E. Sparks3Keigi Fujiwara4Jun-ichi Abe5School of Medicine & Dentistry, Aab Cardiovascular Research Institute, University of Rochester Medical Center, 601 Elmwood Avenue, Box CVRI, Rochester, NY 14642, USASchool of Medicine and Dentistry, the Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 608, Rochester, NY 14642, USASchool of Medicine and Dentistry, the Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 608, Rochester, NY 14642, USASchool of Medicine and Dentistry, the Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 608, Rochester, NY 14642, USASchool of Medicine & Dentistry, Aab Cardiovascular Research Institute, University of Rochester Medical Center, 601 Elmwood Avenue, Box CVRI, Rochester, NY 14642, USASchool of Medicine & Dentistry, Aab Cardiovascular Research Institute, University of Rochester Medical Center, 601 Elmwood Avenue, Box CVRI, Rochester, NY 14642, USAAlthough the exact mechanism through which NADPH oxidases (Nox’s) generate reactive oxygen species (ROS) is still not completely understood, it is widely considered that ROS accumulation is the cause of oxidative stress in endothelial cells. Increasing pieces of evidence strongly indicate the role for ROS in endothelial inflammation and dysfunction and subsequent development of atherosclerotic plaques, which are causes of various pathological cardiac events. An overview for a causative relationship between ROS and endothelial inflammation will be provided in this review. Particularly, a crucial role for specific protein SUMOylation in endothelial inflammation will be presented. Given that SUMOylation of specific proteins leads to increased endothelial inflammation, targeting specific SUMOylated proteins may be an elegant, effective strategy to control inflammation. In addition, the involvement of ROS production in increasing the risk of recurrent coronary events in a sub-group of non-diabetic, post-infarction patients with elevated levels of HDL-cholesterol will be presented with the emphasis that elevated HDL-cholesterol under certain inflammatory conditions can lead to increased incidence of cardiovascular events.http://dx.doi.org/10.1155/2012/678190 |
| spellingShingle | Nhat-Tu Le James P. Corsetti Janet L. Dehoff-Sparks Charles E. Sparks Keigi Fujiwara Jun-ichi Abe Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation International Journal of Inflammation |
| title | Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation |
| title_full | Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation |
| title_fullStr | Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation |
| title_full_unstemmed | Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation |
| title_short | Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation |
| title_sort | reactive oxygen species sumoylation and endothelial inflammation |
| url | http://dx.doi.org/10.1155/2012/678190 |
| work_keys_str_mv | AT nhattule reactiveoxygenspeciessumoylationandendothelialinflammation AT jamespcorsetti reactiveoxygenspeciessumoylationandendothelialinflammation AT janetldehoffsparks reactiveoxygenspeciessumoylationandendothelialinflammation AT charlesesparks reactiveoxygenspeciessumoylationandendothelialinflammation AT keigifujiwara reactiveoxygenspeciessumoylationandendothelialinflammation AT junichiabe reactiveoxygenspeciessumoylationandendothelialinflammation |