Matches in SemOpenAlex for { <https://semopenalex.org/work/W3015200132> ?p ?o ?g. }
- W3015200132 endingPage "101536" @default.
- W3015200132 startingPage "101536" @default.
- W3015200132 abstract "Cardiovascular side effects are frequent problems accompanying systemic glucocorticoid therapy, although the underlying mechanisms are not fully resolved. Reactive oxygen species (ROS) have been shown to promote various cardiovascular diseases although the link between glucocorticoid and ROS signaling has been controversial. As the family of NADPH oxidases has been identified as important source of ROS in the cardiovascular system we investigated the role of NADPH oxidases in response to the synthetic glucocorticoid dexamethasone in the cardiovascular system in vitro and in vivo in mice lacking functional NADPH oxidases due to a mutation in the gene coding for the essential NADPH oxidase subunit p22phox. We show that dexamethasone induced NADPH oxidase-dependent ROS generation, leading to vascular proliferation and angiogenesis due to activation of the transcription factor hypoxia-inducible factor-1 (HIF1). Chronic treatment of mice with low doses of dexamethasone resulted in the development of systemic hypertension, cardiac hypertrophy and left ventricular dysfunction, as well as in pulmonary hypertension and pulmonary vascular remodeling. In contrast, mice deficient in p22phox-dependent NADPH oxidases were protected against these cardiovascular side effects. Mechanistically, dexamethasone failed to upregulate HIF1α levels in these mice, while vascular HIF1α deficiency prevented pulmonary vascular remodeling. Thus, p22phox-dependent NADPH oxidases and activation of the HIF pathway are critical elements in dexamethasone-induced cardiovascular pathologies and might provide interesting targets to limit cardiovascular side effects in patients on chronic glucocorticoid therapy." @default.
- W3015200132 created "2020-04-17" @default.
- W3015200132 creator A5014641684 @default.
- W3015200132 creator A5015844095 @default.
- W3015200132 creator A5023878137 @default.
- W3015200132 creator A5026048159 @default.
- W3015200132 creator A5039882332 @default.
- W3015200132 creator A5055496234 @default.
- W3015200132 creator A5060498574 @default.
- W3015200132 creator A5070350398 @default.
- W3015200132 date "2020-07-01" @default.
- W3015200132 modified "2023-10-14" @default.
- W3015200132 title "NADPH oxidases and HIF1 promote cardiac dysfunction and pulmonary hypertension in response to glucocorticoid excess" @default.
- W3015200132 cites W1211413901 @default.
- W3015200132 cites W1480321196 @default.
- W3015200132 cites W1501198125 @default.
- W3015200132 cites W1510406077 @default.
- W3015200132 cites W1538765821 @default.
- W3015200132 cites W1586099293 @default.
- W3015200132 cites W1593018684 @default.
- W3015200132 cites W164209717 @default.
- W3015200132 cites W176907368 @default.
- W3015200132 cites W1865246179 @default.
- W3015200132 cites W1963339341 @default.
- W3015200132 cites W1965283604 @default.
- W3015200132 cites W1965288097 @default.
- W3015200132 cites W1976980661 @default.
- W3015200132 cites W1983216934 @default.
- W3015200132 cites W1989736478 @default.
- W3015200132 cites W1996597646 @default.
- W3015200132 cites W2002991664 @default.
- W3015200132 cites W2003578638 @default.
- W3015200132 cites W2004396927 @default.
- W3015200132 cites W2012364005 @default.
- W3015200132 cites W2013818100 @default.
- W3015200132 cites W2014187677 @default.
- W3015200132 cites W2014909568 @default.
- W3015200132 cites W2020512725 @default.
- W3015200132 cites W2027762258 @default.
- W3015200132 cites W2028658650 @default.
- W3015200132 cites W2029537954 @default.
- W3015200132 cites W2032264754 @default.
- W3015200132 cites W2033810451 @default.
- W3015200132 cites W2034825883 @default.
- W3015200132 cites W2034836489 @default.
- W3015200132 cites W2037586146 @default.
- W3015200132 cites W2051882452 @default.
- W3015200132 cites W2053616163 @default.
- W3015200132 cites W2059674911 @default.
- W3015200132 cites W2060903877 @default.
- W3015200132 cites W2063902183 @default.
- W3015200132 cites W2072963303 @default.
- W3015200132 cites W2073015829 @default.
- W3015200132 cites W2077036029 @default.
- W3015200132 cites W2077558549 @default.
- W3015200132 cites W2078659604 @default.
- W3015200132 cites W2082033913 @default.
- W3015200132 cites W2083627697 @default.
- W3015200132 cites W2085128107 @default.
- W3015200132 cites W2085727131 @default.
- W3015200132 cites W2086186933 @default.
- W3015200132 cites W2087377825 @default.
- W3015200132 cites W2093962378 @default.
- W3015200132 cites W2094293627 @default.
- W3015200132 cites W2097325814 @default.
- W3015200132 cites W2101022307 @default.
- W3015200132 cites W2101219513 @default.
- W3015200132 cites W2101390983 @default.
- W3015200132 cites W2105192600 @default.
- W3015200132 cites W2110481067 @default.
- W3015200132 cites W2110539420 @default.
- W3015200132 cites W2112155937 @default.
- W3015200132 cites W2112342981 @default.
- W3015200132 cites W2114825476 @default.
- W3015200132 cites W2120261914 @default.
- W3015200132 cites W2120270311 @default.
- W3015200132 cites W2125540025 @default.
- W3015200132 cites W2133203435 @default.
- W3015200132 cites W2137425234 @default.
- W3015200132 cites W2138826820 @default.
- W3015200132 cites W2142310347 @default.
- W3015200132 cites W2147787157 @default.
- W3015200132 cites W2148549438 @default.
- W3015200132 cites W2152414362 @default.
- W3015200132 cites W2157265934 @default.
- W3015200132 cites W2157947474 @default.
- W3015200132 cites W2161767734 @default.
- W3015200132 cites W2162459367 @default.
- W3015200132 cites W2166083608 @default.
- W3015200132 cites W2166381187 @default.
- W3015200132 cites W2167473316 @default.
- W3015200132 cites W2168403919 @default.
- W3015200132 cites W2168574120 @default.
- W3015200132 cites W2169058898 @default.
- W3015200132 cites W2170048907 @default.
- W3015200132 cites W2172084351 @default.
- W3015200132 cites W2178571345 @default.
- W3015200132 cites W2185273348 @default.