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- W3054417943 endingPage "337" @default.
- W3054417943 startingPage "311" @default.
- W3054417943 abstract "Reactive oxygen species (ROS) dysregulation is a hallmark of cardiovascular disease, characterised by an imbalance in the synthesis and removal of ROS. ROS such as superoxide (•O2−), hydrogen peroxide (H2O2), hydroxyl (OH•) and peroxynitrite (ONOO−) have a marked impact on cardiovascular function, contributing to the vascular impairment and cardiac dysfunction associated with diseases such as angina, hypertension, diabetes and heart failure. Central to the vascular dysfunction is a reduction in bioavailability and/or physiological effects of vasoprotective nitric oxide (NO•), leading to vasoconstriction, inflammation and vascular remodelling. In a cardiac context, increased ROS generation can also lead to modification of key proteins involved in cardiac contractility. Whilst playing a key role in the pathogenesis of cardiovascular disease, ROS dysregulation also limits the clinical efficacy of current therapies, such as nitrosovasodilators. As such, alternate therapies are sought. This review will discuss the impact of ROS dysregulation on the therapeutic utility of NO• and its redox sibling, nitroxyl (HNO)." @default.
- W3054417943 created "2020-08-24" @default.
- W3054417943 creator A5000981149 @default.
- W3054417943 creator A5010660115 @default.
- W3054417943 creator A5028734833 @default.
- W3054417943 creator A5068741420 @default.
- W3054417943 creator A5069893866 @default.
- W3054417943 date "2020-01-01" @default.
- W3054417943 modified "2023-10-01" @default.
- W3054417943 title "Cardiovascular Therapeutic Potential of the Redox Siblings, Nitric Oxide (NO•) and Nitroxyl (HNO), in the Setting of Reactive Oxygen Species Dysregulation" @default.
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