Targeting microglia-mediated neurotoxicity: the potential of NOX2 inhibitors - PubMed (original) (raw)
Review
Targeting microglia-mediated neurotoxicity: the potential of NOX2 inhibitors
Michael J Surace et al. Cell Mol Life Sci. 2012 Jul.
Abstract
Microglia are key sentinels of central nervous system health, and their dysfunction has been widely implicated in the progressive nature of neurodegenerative diseases. While microglia can produce a host of factors that are toxic to neighboring neurons, NOX2 has been implicated as a common and essential mechanism of microglia-mediated neurotoxicity. Accumulating evidence indicates that activation of the NOX2 enzyme complex in microglia is neurotoxic, both through the production of extracellular reactive oxygen species that damage neighboring neurons as well as the initiation of redox signaling in microglia that amplifies the pro-inflammatory response. More specifically, evidence supports that NOX2 redox signaling enhances microglial sensitivity to pro-inflammatory stimuli, and amplifies the production of neurotoxic cytokines, to promote chronic and neurotoxic microglial activation. Here, we describe the evidence denoting the role of NOX2 in microglia-mediated neurotoxicity with an emphasis on Alzheimer's and Parkinson's disease, describe available inhibitors that have been tested, and detail evidence of the neuroprotective and therapeutic potential of targeting this enzyme complex to regulate microglia.
Figures
Fig. 1
NOX2 is key for neurotoxic microglial activation. Microglial NOX2 is activated by cytokines, endogenous disease proteins, inflammogens, and soluble neuron injury signals from neuron death/damage (reactive microglisosis), which is implicated in self-propagating neurotoxicity. Thus, specific inhibition of NOX2 is a promising target with the potential to break the cycle of chronic and neurotoxic microglial activation that is implicated in the progressive nature of neurodegenerative diseases
Fig. 2
Inhibitors target microglial NOX2 activation through two mechanisms. Activation of the NOX2 complex occurs in microglia in response to several stimuli and multiple signaling pathways, where activation is due to the assembly of the enzyme complex, as depicted here. Several putative NOX2 inhibitors have been identified that attenuate microglial activation to confer neuroprotection. Here, we classify compounds that have been shown to inhibit microglial NOX2 activity into one of two categories based on whether the molecules were: (1) proposed to directly inhibit the catalytic subunit or (2) indirectly modulate NOX2 through inhibition of phosporylation and translocation of cytosolic subunits or other pathways. Notably, most of these molecules are not specific for NOX2 and the mechanism of NOX2 inhibition are either poorly understood or unknown at this time
Similar articles
- NOX2 As a Target for Drug Development: Indications, Possible Complications, and Progress.
Diebold BA, Smith SM, Li Y, Lambeth JD. Diebold BA, et al. Antioxid Redox Signal. 2015 Aug 10;23(5):375-405. doi: 10.1089/ars.2014.5862. Epub 2014 Mar 24. Antioxid Redox Signal. 2015. PMID: 24512192 Free PMC article. Review. - Clozapine metabolites protect dopaminergic neurons through inhibition of microglial NADPH oxidase.
Jiang L, Wu X, Wang S, Chen SH, Zhou H, Wilson B, Jin CY, Lu RB, Xie K, Wang Q, Hong JS. Jiang L, et al. J Neuroinflammation. 2016 May 16;13(1):110. doi: 10.1186/s12974-016-0573-z. J Neuroinflammation. 2016. PMID: 27184631 Free PMC article. - NADPH oxidase 2-derived reactive oxygen species in the hippocampus might contribute to microglial activation in postoperative cognitive dysfunction in aged mice.
Qiu LL, Ji MH, Zhang H, Yang JJ, Sun XR, Tang H, Wang J, Liu WX, Yang JJ. Qiu LL, et al. Brain Behav Immun. 2016 Jan;51:109-118. doi: 10.1016/j.bbi.2015.08.002. Epub 2015 Aug 4. Brain Behav Immun. 2016. PMID: 26254234 - Role and mechanism of microglial activation in iron-induced selective and progressive dopaminergic neurodegeneration.
Zhang W, Yan ZF, Gao JH, Sun L, Huang XY, Liu Z, Yu SY, Cao CJ, Zuo LJ, Chen ZJ, Hu Y, Wang F, Hong JS, Wang XM. Zhang W, et al. Mol Neurobiol. 2014 Jun;49(3):1153-65. doi: 10.1007/s12035-013-8586-4. Epub 2013 Nov 26. Mol Neurobiol. 2014. PMID: 24277523 Free PMC article. - NADPH oxidase as a therapeutic target in Alzheimer's disease.
Block ML. Block ML. BMC Neurosci. 2008 Dec 3;9 Suppl 2(Suppl 2):S8. doi: 10.1186/1471-2202-9-S2-S8. BMC Neurosci. 2008. PMID: 19090996 Free PMC article. Review.
Cited by
- NOX2 As a Target for Drug Development: Indications, Possible Complications, and Progress.
Diebold BA, Smith SM, Li Y, Lambeth JD. Diebold BA, et al. Antioxid Redox Signal. 2015 Aug 10;23(5):375-405. doi: 10.1089/ars.2014.5862. Epub 2014 Mar 24. Antioxid Redox Signal. 2015. PMID: 24512192 Free PMC article. Review. - Sex differences in microglial phagocytosis in the neonatal hippocampus.
Nelson LH, Warden S, Lenz KM. Nelson LH, et al. Brain Behav Immun. 2017 Aug;64:11-22. doi: 10.1016/j.bbi.2017.03.010. Epub 2017 Mar 22. Brain Behav Immun. 2017. PMID: 28341582 Free PMC article. - Postnatal Antioxidant and Anti-inflammatory Treatments Prevent Early Ketamine-Induced Cortical Dysfunctions in Adult Mice.
Bove M, Tucci P, Dimonte S, Trabace L, Schiavone S, Morgese MG. Bove M, et al. Front Neurosci. 2020 Nov 4;14:590088. doi: 10.3389/fnins.2020.590088. eCollection 2020. Front Neurosci. 2020. PMID: 33250707 Free PMC article. - Homeostatic interferon expression in neurons is sufficient for early control of viral infection.
Cavanaugh SE, Holmgren AM, Rall GF. Cavanaugh SE, et al. J Neuroimmunol. 2015 Feb 15;279:11-9. doi: 10.1016/j.jneuroim.2014.12.012. Epub 2014 Dec 16. J Neuroimmunol. 2015. PMID: 25669994 Free PMC article. - The Antioxidant, Anti-Inflammatory, and Neuroprotective Properties of the Synthetic Chalcone Derivative AN07.
Chen YF, Wu SN, Gao JM, Liao ZY, Tseng YT, Fülöp F, Chang FR, Lo YC. Chen YF, et al. Molecules. 2020 Jun 24;25(12):2907. doi: 10.3390/molecules25122907. Molecules. 2020. PMID: 32599797 Free PMC article.
References
- Mittelbronn M, et al. Local distribution of microglia in the normal adult human central nervous system differs by up to one order of magnitude. Acta Neuropathol (Berl) 2001;101(3):249–255. - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous