Titlebook: Reactive Oxygen Species; Network Pharmacology Harald H. H. W. Schmidt,Pietro Ghezzi,Antonio Cuad Book 2021 Springer Nature Switzerland AG 2

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Oxidants in Physiological Processesventions that target persistently altered ROS levels should include both selective inhibition of a specific source of primary ROS and careful consideration of a targeted pro-oxidant approach, an avenue that is still underdeveloped. Both strategies require attention to redox dynamics in complex cellu

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Network Medicine-Based Unbiased Disease Modules for Drug and Diagnostic Target Identification in ROSringent subnet participation degree (SPD) of 0.4, hub nodes excluded. This resulted in 12 distinct human interactome-based ROS signalling modules, while 8 proteins remaining unconnected. This ROSome is in sharp contrast to commonly used highly curated and integrated KEGG, HMDB or WikiPathways. These

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Nitric Oxide Synthase Inhibitors into the Clinic at Lasteclining in clinical relevance or hold promise but need yet to enter formal therapeutic guidelines, respectively. Nevertheless, NOS inhibition in situations of NO overproduction often jointly with enhanced superoxide (or hydrogen peroxide production) still holds promise, but most likely only in acut

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Effects of Mammalian Thioredoxin Reductase Inhibitorscancer efficacy. The observed increases in antioxidant capacity upon inhibition of TrxR in normal cells are in part dependent upon activation of the Nrf2 transcription factor, while exaggerated ROS levels in cancer cells can be explained by a non-oncogene addiction of cancer cells to TrxR1 due to th

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Cardiovascular Therapeutic Potential of the Redox Siblings, Nitric Oxide (NO?) and Nitroxyl (HNO), icy 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)..Both nitric oxide (NO) and nitroxyl (HNO) donors signal through soluble gua

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Tetrahydrobiopterin and Nitric Oxide Synthase Recouplerstor, tetrahydrobiopterin (BH4). The duality of NOS functions as enzymes that generate both NO and ROS under different regulatory states has emerged as an important pathophysiologic mechanism, and is a potential therapeutic target, via agents that can maintain or restore NOS coupling, for example via