NOX Enzymes in the Central Nervous System: From Signaling to Disease

Sorce, Silvia; Krause, Karl‐Heinz

doi:10.1089/ars.2009.2578

Cited by 411 publications

(363 citation statements)

References 273 publications

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“…Moreover, ROS contribute to neuronal apoptosis, which is a key mechanism in brain development. 53 Furthermore, ROS can regulate neuronal ion channels, kinases, and transcription factors. 54,55 ROS generated from the NADPH oxidase 2 (Nox2) system also contribute to long-term memory dysfunction.…”

Section: Oxidative Stressmentioning

confidence: 99%

Central nervous system toxicity of metallic nanoparticles

Feng¹,

Chen²,

Zhang³

et al. 2015

IJN

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Nanomaterials (NMs) are increasingly used for the therapy, diagnosis, and monitoring of disease- or drug-induced mechanisms in the human biological system. In view of their small size, after certain modifications, NMs have the capacity to bypass or cross the blood–brain barrier. Nanotechnology is particularly advantageous in the field of neurology. Examples may include the utilization of nanoparticle (NP)-based drug carriers to readily cross the blood–brain barrier to treat central nervous system (CNS) diseases, nanoscaffolds for axonal regeneration, nanoelectromechanical systems in neurological operations, and NPs in molecular imaging and CNS imaging. However, NPs can also be potentially hazardous to the CNS in terms of nano-neurotoxicity via several possible mechanisms, such as oxidative stress, autophagy, and lysosome dysfunction, and the activation of certain signaling pathways. In this review, we discuss the dual effect of NMs on the CNS and the mechanisms involved. The limitations of the current research are also discussed.

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Section: Oxidative Stressmentioning

confidence: 99%

Central nervous system toxicity of metallic nanoparticles

Feng¹,

Chen²,

Zhang³

et al. 2015

IJN

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“…In addition to NOX2, microglia have been shown to express functional NOX1 [12] and NOX4 [13]. Furthermore, NOX1, NOX2, and NOX4 are expressed in neurons, astrocytes, endothelial cells, pericytes and fibroblasts, among other cells [14,15]. For the purpose of this review, we will focus on NOX2, but some of the research and therapy approaches may overlap with NOX1 and NOX4.…”

Section: Nadph Oxidasementioning

confidence: 99%

Novel Neuroinflammatory Targets in the Chronically Injured Spinal Cord

Pajoohesh‐Ganji

Byrnes

2011

Neurotherapeutics

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Summary: Injury to the spinal cord is known to result in inflammation. To date, the preponderance of research has focused on the acute neuroinflammatory response, which begins immediately and is believed to terminate within hours to (at most) days after the injury. However, recent studies have demonstrated that postinjury inflammation is not restricted to the first few hours or days after injury, but can last for months to years after a spinal cord injury (SCI). These chronic studies have revealed that increased numbers of inflammatory cells, such as microglia and macrophages, and inflammatory factors, including cytokines, chemokines, and enzyme products are found at markedly delayed times after injury. Here we review experimental work on a selection of the novel inflammatory factors observed chronically after SCI, including the nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) oxidase enzyme and galectin-3. We will discuss the role of these proteins in inflammation with regard to both detrimental and beneficial effects of neuroinflammation after injury. Finally, the potential of these proteins to serve as therapeutic targets will be considered, and a novel therapeutic approach (i.e., the agonist for metabotropic glutamate receptor 5 [mGluR5], [RS]-2-Chloro-5-hydroxyphenylglycine [CHPG]) will be discussed. This review will demonstrate the expression and activity profiles, roles in potentiation of injury, and therapy studies of these inflammatory factors suggest that not only are these chronically expressed factors viable targets for SCI treatment, but that the therapeutic window is broader than has previously been thought.

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“…Mitochondrial sources of ROS include the electron transport chain, matrix dehydrogenases, free iron, and monoamine oxidases (Andreyev et al, 2005;Horowitz and Greenamyre, 2010). Numerous extramitochondrial sources of ROS and reactive nitrogen species include inducible NADPH oxidase, which is particularly important in the oxidative stress associated with cellular inflammatory activities (Sorce and Krause, 2009). Mitochondrial targets for damage by ROS and reactive nitrogen species include electron transport chain components, tricarboxylic Figure 1 Mitochondrial mechanisms of neural cell death and targets for neuroprotection.…”

Section: Introductionmentioning

confidence: 99%

Novel Mitochondrial Targets for Neuroprotection

Pérez-Pinzón

Stetler

Fiskum

2012

J Cereb Blood Flow Metab

130

108

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Mitochondrial dysfunction contributes to the pathophysiology of acute neurologic disorders and neurodegenerative diseases. Bioenergetic failure is the primary cause of acute neuronal necrosis, and involves excitotoxicity-associated mitochondrial Ca 2 + overload, resulting in opening of the inner membrane permeability transition pore and inhibition of oxidative phosphorylation. Mitochondrial energy metabolism is also very sensitive to inhibition by reactive O 2 and nitrogen species, which modify many mitochondrial proteins, lipids, and DNA/RNA, thus impairing energy transduction and exacerbating free radical production. Oxidative stress and Ca 2 + -activated calpain protease activities also promote apoptosis and other forms of programmed cell death, primarily through modification of proteins and lipids present at the outer membrane, causing release of proapoptotic mitochondrial proteins, which initiate caspase-dependent and caspase-independent forms of cell death. This review focuses on three classifications of mitochondrial targets for neuroprotection. The first is mitochondrial quality control, maintained by the dynamic processes of mitochondrial fission and fusion and autophagy of abnormal mitochondria. The second includes targets amenable to ischemic preconditioning, e.g., electron transport chain components, ion channels, uncoupling proteins, and mitochondrial biogenesis. The third includes mitochondrial proteins and other molecules that defend against oxidative stress. Each class of targets exhibits excellent potential for translation to clinical neuroprotection.

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NOX Enzymes in the Central Nervous System: From Signaling to Disease

Cited by 411 publications

References 273 publications

Central nervous system toxicity of metallic nanoparticles

Central nervous system toxicity of metallic nanoparticles

Novel Neuroinflammatory Targets in the Chronically Injured Spinal Cord

Novel Mitochondrial Targets for Neuroprotection

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