Matches in SemOpenAlex for { <https://semopenalex.org/work/W1965891907> ?p ?o ?g. }
- W1965891907 endingPage "1606" @default.
- W1965891907 startingPage "1583" @default.
- W1965891907 abstract "Excessive reactive oxygen species Revised abstract, especially superoxide anion (O₂•-), play important roles in the pathogenesis of many cardiovascular diseases, including hypertension and atherosclerosis. Superoxide dismutases (SODs) are the major antioxidant defense systems against (O₂•-), which consist of three isoforms of SOD in mammals: the cytoplasmic Cu/ZnSOD (SOD1), the mitochondrial MnSOD (SOD2), and the extracellular Cu/ZnSOD (SOD3), all of which require catalytic metal (Cu or Mn) for their activation. Recent evidence suggests that in each subcellular location, SODs catalyze the conversion of (O₂•-), H2O2, which may participate in cell signaling. In addition, SODs play a critical role in inhibiting oxidative inactivation of nitric oxide, thereby preventing peroxynitrite formation and endothelial and mitochondrial dysfunction. The importance of each SOD isoform is further illustrated by studies from the use of genetically altered mice and viral-mediated gene transfer. Given the essential role of SODs in cardiovascular disease, the concept of antioxidant therapies, that is, reinforcement of endogenous antioxidant defenses to more effectively protect against oxidative stress, is of substantial interest. However, the clinical evidence remains controversial. In this review, we will update the role of each SOD in vascular biologies, physiologies, and pathophysiologies such as atherosclerosis, hypertension, and angiogenesis. Because of the importance of metal cofactors in the activity of SODs, we will also discuss how each SOD obtains catalytic metal in the active sites. Finally, we will discuss the development of future SOD-dependent therapeutic strategies." @default.
- W1965891907 created "2016-06-24" @default.
- W1965891907 creator A5021137697 @default.
- W1965891907 creator A5085309946 @default.
- W1965891907 date "2011-09-15" @default.
- W1965891907 modified "2023-10-18" @default.
- W1965891907 title "Superoxide Dismutases: Role in Redox Signaling, Vascular Function, and Diseases" @default.
- W1965891907 cites W103480297 @default.
- W1965891907 cites W1516659005 @default.
- W1965891907 cites W1525061277 @default.
- W1965891907 cites W1528220495 @default.
- W1965891907 cites W1528247040 @default.
- W1965891907 cites W1533514289 @default.
- W1965891907 cites W1534322556 @default.
- W1965891907 cites W1573826674 @default.
- W1965891907 cites W1580575515 @default.
- W1965891907 cites W1585758755 @default.
- W1965891907 cites W1679832876 @default.
- W1965891907 cites W1710550832 @default.
- W1965891907 cites W1748754899 @default.
- W1965891907 cites W1769875470 @default.
- W1965891907 cites W1802861244 @default.
- W1965891907 cites W1899087901 @default.
- W1965891907 cites W1921965616 @default.
- W1965891907 cites W1925799544 @default.
- W1965891907 cites W1940436875 @default.
- W1965891907 cites W1963874808 @default.
- W1965891907 cites W1964590720 @default.
- W1965891907 cites W1965770783 @default.
- W1965891907 cites W1967637508 @default.
- W1965891907 cites W1969087884 @default.
- W1965891907 cites W1969706519 @default.
- W1965891907 cites W1970094644 @default.
- W1965891907 cites W1970382485 @default.
- W1965891907 cites W1971326367 @default.
- W1965891907 cites W1971510408 @default.
- W1965891907 cites W1972415780 @default.
- W1965891907 cites W1972467026 @default.
- W1965891907 cites W1973376761 @default.
- W1965891907 cites W1974126557 @default.
- W1965891907 cites W1975356402 @default.
- W1965891907 cites W1975927777 @default.
- W1965891907 cites W1976616659 @default.
- W1965891907 cites W1978214583 @default.
- W1965891907 cites W1978423213 @default.
- W1965891907 cites W1978425164 @default.
- W1965891907 cites W1978490949 @default.
- W1965891907 cites W1978640785 @default.
- W1965891907 cites W1980842796 @default.
- W1965891907 cites W1981119259 @default.
- W1965891907 cites W1983045014 @default.
- W1965891907 cites W1983229253 @default.
- W1965891907 cites W1983755918 @default.
- W1965891907 cites W1983760621 @default.
- W1965891907 cites W1986454658 @default.
- W1965891907 cites W1988087076 @default.
- W1965891907 cites W1989726385 @default.
- W1965891907 cites W1995528647 @default.
- W1965891907 cites W1996296598 @default.
- W1965891907 cites W1996797097 @default.
- W1965891907 cites W1997595809 @default.
- W1965891907 cites W1998934871 @default.
- W1965891907 cites W1999649376 @default.
- W1965891907 cites W1999721769 @default.
- W1965891907 cites W1999825318 @default.
- W1965891907 cites W2000428946 @default.
- W1965891907 cites W2001848039 @default.
- W1965891907 cites W2003259342 @default.
- W1965891907 cites W2003276934 @default.
- W1965891907 cites W2003744390 @default.
- W1965891907 cites W2004557982 @default.
- W1965891907 cites W2007277298 @default.
- W1965891907 cites W2008837541 @default.
- W1965891907 cites W2008970981 @default.
- W1965891907 cites W2009046724 @default.
- W1965891907 cites W2009554048 @default.
- W1965891907 cites W2010110222 @default.
- W1965891907 cites W2011007124 @default.
- W1965891907 cites W2011988006 @default.
- W1965891907 cites W2012584055 @default.
- W1965891907 cites W2013311895 @default.
- W1965891907 cites W2014802937 @default.
- W1965891907 cites W2017199287 @default.
- W1965891907 cites W2020000452 @default.
- W1965891907 cites W2020333559 @default.
- W1965891907 cites W2021276746 @default.
- W1965891907 cites W2022222328 @default.
- W1965891907 cites W2022584313 @default.
- W1965891907 cites W2024301095 @default.
- W1965891907 cites W2026433593 @default.
- W1965891907 cites W2026587757 @default.
- W1965891907 cites W2027043097 @default.
- W1965891907 cites W2028661305 @default.
- W1965891907 cites W2031729422 @default.
- W1965891907 cites W2036278497 @default.
- W1965891907 cites W2037434205 @default.
- W1965891907 cites W2037864697 @default.
- W1965891907 cites W2038284767 @default.