A Mini-Review of the NADPH Oxidases in Vascular Dementia: Correlation with NOXs and Risk Factors for VaD

Choi, Dong‐Hee; Lee, Jongmin

doi:10.3390/ijms18112500

Cited by 28 publications

(22 citation statements)

References 140 publications

(196 reference statements)

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“…The physiologic functions of these enzymes include host defense, regulation of gene expression, and cell differentiation. It is becoming increasing clear that NOX activity is elevated in several neurodegenerative conditions and inhibition or genetic deletion of these enzymes has therapeutic benefits (37,94,95,377,476,544).…”

Section: B Sources Of Ros Generationmentioning

confidence: 99%

Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities

Sbodio

Snyder

Paul

2019

Antioxidants & Redox Signaling

108

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Due to the importance of redox control in physiologic processes, organisms have evolved multiple pathways to counteract redox imbalance and maintain homeostasis. Cells and tissues address stress by harnessing an array of both endogenous and exogenous redox active substances. Targeting these pathways can help mitigate symptoms associated with neurodegeneration and may provide avenues for novel therapeutics. Antioxid. Redox Signal. 00, 000-000.

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Section: B Sources Of Ros Generationmentioning

confidence: 99%

Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities

Sbodio

Snyder

Paul

2019

Antioxidants & Redox Signaling

108

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“…On the other hand, chronic activation of NADPH oxidases has been implicated in a broad spectrum of age-dependent pathologies. For instance, during aging, the ROS from Nox1, 2, 4 contribute to molecular damage of the vascular system, potentially leading to hypertension, stroke, neuroinflammation, and dementia [ 84 , 85 ]. Furthermore, during aging, the Nox2 expression levels as well as Rac1 protein levels increase, leading to increased ROS levels driving cardiomyocyte hypertrophy and fibrosis in the aging hearts of rats [ 86 ].…”

Section: The Role Of Nadph Oxidases During Mammalian Agingmentioning

confidence: 99%

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging

Ewald

2018

Antioxidants

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An accumulating body of evidence suggests that transient or physiological reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases act as a redox signal to re-establish homeostasis. The capacity to re-establish homeostasis progressively declines during aging but is maintained in long-lived animals to promote healthy aging. In the model organism Caenorhabditis elegans, ROS generated by dual oxidases (Duox) are important for extracellular matrix integrity, pathogen defense, oxidative stress resistance, and longevity. The Duox enzymatic activity is tightly regulated and under cellular control. Developmental molting cycles, pathogen infections, toxins, mitochondrial-derived ROS, drugs, and small GTPases (e.g., RHO-1) can activate Duox (BLI-3) to generate ROS, whereas NADPH oxidase inhibitors and negative regulators, such as MEMO-1, can inhibit Duox from generating ROS. Three mechanisms-of-action have been discovered for the Duox/BLI-3-generated ROS: (1) enzymatic activity to catalyze crosslinking of free tyrosine ethyl ester in collagen bundles to stabilize extracellular matrices, (2) high ROS bursts/levels to kill pathogens, and (3) redox signaling activating downstream kinase cascades to transcription factors orchestrating oxidative stress and immunity responses to re-establish homeostasis. Although Duox function at the cell surface is well established, recent genetic and biochemical data also suggests a novel role for Duoxs at the endoplasmic reticulum membrane to control redox signaling. Evidence underlying these mechanisms initiated by ROS from NADPH oxidases, and their relevance for human aging, are discussed in this review. Appropriately controlling NADPH oxidase activity for local and physiological redox signaling to maintain cellular homeostasis might be a therapeutic strategy to promote healthy aging.

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“…The mentioned chemical reactions are presented in Figure 3. The superoxide itself can be formed in various ways from which the reaction mediated by NADPH oxidase appears as a relevant one while the association between NADPH oxidase expression and neuropathologies including Alzheimer disease is also deeply investigated (84,85). The peroxinitrite is a cytotoxic compound given to a wider group of reactive oxygen and nitrogen species and a signifi cant contributor to oxidative stress (86)(87)(88).…”

Section: Metabolism As a Source Of Reactive Compoundsmentioning

confidence: 99%

Oxidative stress in Alzheimer disease as a target for therapy

Pohanka¹

2018

BLL

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In the recent time, neurodegenerative disorders like Alzheimer disease were recognized for their significant role in the current healthcare because of their growing incidence and costs for health insurance systems. Effective therapy is missing and even etiology of the diseases like Alzheimer disease is not deeply known. In the case of Alzheimer disease, it is probable that oxidative stress is at least a factor involved in the disease. Nevertheless, the current literature is controversial and ambiguous in this matter. This review is focused on mapping the role of oxidative stress as well as on a consideration that oxidative stress represents the pathway at which a therapeutic strategy can be aimed. This paper provides a survey of contemporary literature on oxidative stress in Alzheimer disease and discusses the opportunities for establishing a therapy based on interfering the stress (Fig. 5, Ref. 117).

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A Mini-Review of the NADPH Oxidases in Vascular Dementia: Correlation with NOXs and Risk Factors for VaD

Cited by 28 publications

References 140 publications

Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities

Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging

Oxidative stress in Alzheimer disease as a target for therapy

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