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- W2573662277 startingPage "203" @default.
- W2573662277 abstract "Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are produced under physiological conditions as innocent by-products and serve as useful redox signalling molecules. An advanced set of endogenous antioxidants safely handle these reactive species, which allows for them to be utilized by our cells and tissues. In many diseases, including ischaemic stroke, this fine balance is shifted so that our antioxidants are outnumbered by ROS and RNS; this results in oxidative stress, which can lead to toxicity and cell death with severe and potentially lethal consequences for the individual. Oxidative stress plays a crucial and central role in the pathophysiological cascade responsible for brain damage following a stroke by mediating severe toxicity in the acute phase and initiating and contributing to late-stage apoptosis and inflammation. This review will describe the chemistry, biochemical sources, and harmful effects of ROS/RNS in order to provide insight into the diverse and complex elements of oxidative stress. Then, oxidative stress’ relationship to ischaemic stroke will be addressed, with a focus on the biochemical mechanisms that lead to neurotoxicity. Pharmacological strategies to inhibit oxidative stress in cerebral ischaemia are discussed, including examples that cover past and present efforts. Three potential drug targets against oxidative stress and ischaemic stroke are highlighted, namely PSD-95, NADPH oxidase, and Keap1, and the potential of multi-target drug discovery in relation to ischaemic stroke is outlined." @default.
- W2573662277 created "2017-01-26" @default.
- W2573662277 creator A5059275377 @default.
- W2573662277 date "2017-01-01" @default.
- W2573662277 modified "2023-09-23" @default.
- W2573662277 title "Targeting Oxidative Stress in Stroke" @default.
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