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• W2040831177 endingPage "182" @default.
• W2040831177 startingPage "170" @default.
• W2040831177 abstract "Inducible nitric oxide synthase (iNOS) is one of three NOS isoforms generating nitric oxide (NO) by the conversion of l-arginine to l-citrulline. iNOS has been found to be a major contributor to initiation/exacerbation of the central nervous system (CNS) inflammatory/degenerative conditions through the production of excessive NO which generates reactive nitrogen species (RNSs). Activation of iNOS and NO generation has come to be accepted as a marker and therapeutic target in neuroinflammatory conditions such as those observed in ischemia, multiple sclerosis (MS), spinal cord injury (SCI), Alzheimer's disease (AD), and inherited peroxisomal (e.g. X-linked adrenoleukodystrophy; X-ALD) and lysosomal disorders (e.g. Krabbe's disease). However, with the emergence of reports on the neuroprotective facets of NO, the prior dogma about NO being solely detrimental has had to be modified. While RNSs such as peroxynitrite (ONOO−) have been linked to lipid peroxidation, neuronal/oligodendrocyte loss, and demyelination in neurodegenerative diseases, limited NO generation by GSNO has been found to promote vasodilation and attenuate vascular injury under the same ischemic conditions. NO generated from GSNO acts as second messenger molecular which through S-nitrosylation has been shown to control important cellular processes by regulation of expression/activity of certain proteins such as NF-κB. It is now believed that the environment and the context in which NO is produced largely determines the actions (good or bad) of this molecule. These multi-faceted aspects of NO make therapeutic interference with iNOS activity even more complicated since complete ablation of iNOS activity has been found to be rather more detrimental than protective in most neurodegenerative conditions. Investigators in search of iNOS modulating pharmacological agents have realized the need of a delicate balance so as to allow the production of physiologically relevant amounts of NO (such as those required for host defence/neutotransmission/vasodilation, etc.) but at the same time block the generation of RNSs through repressing excessive NO levels (such as those causing neuronal/tissue damage and demyelination, etc.). The past years have seen a noteworthy increase in novel agents that might prove useful in achieving the aim of harnessing the good and blocking the undesirable actions of NO. It is the aim of this review to provide basic insights into the NOS family of enzymes with special emphasis of the role of iNOS in the CNS, in the first part. In the second part of the review, we will strive to provide an exhaustive compilation of the prevalent strategies being tested for the therapeutic modulation of iNOS and NO production." @default.
• W2040831177 created "2016-06-24" @default.
• W2040831177 creator A5032747758 @default.
• W2040831177 creator A5074841685 @default.
• W2040831177 date "2006-07-01" @default.
• W2040831177 modified "2023-09-26" @default.
• W2040831177 title "Pharmacological strategies for the regulation of inducible nitric oxide synthase: Neurodegenerative versus neuroprotective mechanisms" @default.
• W2040831177 cites W1492776605 @default.
• W2040831177 cites W1497064282 @default.
• W2040831177 cites W1500094754 @default.
• W2040831177 cites W1507107301 @default.
• W2040831177 cites W1528588273 @default.
• W2040831177 cites W1551967777 @default.
• W2040831177 cites W1558213119 @default.
• W2040831177 cites W1565979608 @default.
• W2040831177 cites W1591881963 @default.
• W2040831177 cites W1633340712 @default.
• W2040831177 cites W1639924204 @default.
• W2040831177 cites W1684025987 @default.
• W2040831177 cites W1754891924 @default.
• W2040831177 cites W1764308599 @default.
• W2040831177 cites W1765591388 @default.
• W2040831177 cites W1766190906 @default.
• W2040831177 cites W1805879606 @default.
• W2040831177 cites W1812573520 @default.
• W2040831177 cites W1821918060 @default.
• W2040831177 cites W1834041853 @default.
• W2040831177 cites W1923894350 @default.
• W2040831177 cites W1932535232 @default.
• W2040831177 cites W1954930651 @default.
• W2040831177 cites W1964390249 @default.
• W2040831177 cites W1965476204 @default.
• W2040831177 cites W1967712758 @default.
• W2040831177 cites W1969530182 @default.
• W2040831177 cites W1972926770 @default.
• W2040831177 cites W1973018387 @default.
• W2040831177 cites W1973553450 @default.
• W2040831177 cites W1973671786 @default.
• W2040831177 cites W1976851726 @default.
• W2040831177 cites W1979230311 @default.
• W2040831177 cites W1982361047 @default.
• W2040831177 cites W1983947718 @default.
• W2040831177 cites W1984847566 @default.
• W2040831177 cites W1985049657 @default.
• W2040831177 cites W1990278643 @default.
• W2040831177 cites W1990798856 @default.
• W2040831177 cites W1993735050 @default.
• W2040831177 cites W1995277420 @default.
• W2040831177 cites W1995311216 @default.
• W2040831177 cites W1996267589 @default.
• W2040831177 cites W2004659594 @default.
• W2040831177 cites W2005515164 @default.
• W2040831177 cites W2005879992 @default.
• W2040831177 cites W2007437940 @default.
• W2040831177 cites W2011730327 @default.
• W2040831177 cites W2011769338 @default.
• W2040831177 cites W2012879657 @default.
• W2040831177 cites W2013021682 @default.
• W2040831177 cites W2015848852 @default.
• W2040831177 cites W2016706063 @default.
• W2040831177 cites W2017885661 @default.
• W2040831177 cites W2021179770 @default.
• W2040831177 cites W2021334430 @default.
• W2040831177 cites W2021602447 @default.
• W2040831177 cites W2022699060 @default.
• W2040831177 cites W2024815156 @default.
• W2040831177 cites W2026224903 @default.
• W2040831177 cites W2028877394 @default.
• W2040831177 cites W2029020003 @default.
• W2040831177 cites W2029438492 @default.
• W2040831177 cites W2031650186 @default.
• W2040831177 cites W2032890774 @default.
• W2040831177 cites W2036020592 @default.
• W2040831177 cites W2038227076 @default.
• W2040831177 cites W2038814798 @default.
• W2040831177 cites W2044900347 @default.
• W2040831177 cites W2044930099 @default.
• W2040831177 cites W2045174329 @default.
• W2040831177 cites W2046166342 @default.
• W2040831177 cites W2046366184 @default.
• W2040831177 cites W2049054934 @default.
• W2040831177 cites W2049593742 @default.
• W2040831177 cites W2052078119 @default.
• W2040831177 cites W2055402818 @default.
• W2040831177 cites W2058137293 @default.
• W2040831177 cites W2058436815 @default.
• W2040831177 cites W2059379142 @default.
• W2040831177 cites W2060980402 @default.
• W2040831177 cites W2061569035 @default.
• W2040831177 cites W2063680573 @default.
• W2040831177 cites W2063738580 @default.
• W2040831177 cites W2064167798 @default.
• W2040831177 cites W2064633417 @default.
• W2040831177 cites W2065451295 @default.
• W2040831177 cites W2065705538 @default.
• W2040831177 cites W2067124986 @default.
• W2040831177 cites W2067931227 @default.
• W2040831177 cites W2068751000 @default.

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