Nox/Duox Family of NADPH Oxidases: Lessons from Knockout Mouse Models

Sirokmány, Gábor; Donkó, Ágnes; Geiszt, Miklós

doi:10.1016/j.tips.2016.01.006

Cited by 113 publications

(78 citation statements)

References 68 publications

(90 reference statements)

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“…In order to determine the effect of a lack of Nox4 activity on the homeostasis of bone and how that might elucidate the role of Nox4 in early structural changes to the joint after injury, we performed a characterization and comparison of structural and mechanical properties of bones from WT and Nox4 KO mice. The KO mice had no gross phenotype, which is in accordance with previous studies . KO mice had significantly decreased epiphyseal and metaphyseal BV/TV and trabecular number, with increased trabecular thickness in the epiphysis, and increased TMD in the mid‐diaphysis (Fig.…”

Section: Resultssupporting

confidence: 90%

Acute Changes in NADPH Oxidase 4 in Early Post‐Traumatic Osteoarthritis

Wegner

Campos

Robbins

et al. 2019

Journal Orthopaedic Research

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Knee injuries cause structural damage and acute inflammation that initiates the development of post‐traumatic osteoarthritis (PTOA). NADPH oxidase 4 (Nox4), a member of a family of enzymes that generates reactive oxygen species (ROS), plays a pivotal role in normal development of the musculoskeletal system, but may increase ROS production to harmful levels after joint injury. The role of ROS in both normal joint homeostasis and injury is poorly understood, but inhibition of excessive ROS production by Nox4 after joint injury could be protective to the joint, decreasing oxidative stress, and initiation of PTOA. Knee injuries were simulated using inflammatory cytokines in cultured primary human chondrocytes and a non‐invasive mouse model of PTOA in C57BL/6N and Nox4 knockout mice. There is an acute decrease in Nox4 activity within 24 h after injury in both systems, followed by a subsequent sustained low‐level increase, a novel finding not seen in any other system. Inhibition of Nox4 activity by GKT137831 was protective against early structural changes after non‐invasive knee injury in a mouse model. Nox4 knockout mice had significant differences in structural and mechanical properties of bone, providing further evidence for the role of Nox4 in development of joint tissues and biochemical response after joint injury. Nox4 plays a significant role in the acute phase after joint injury, and targeted inhibition of inflammation caused by Nox4 may be protective against early joint changes in the pathogenesis of PTOA. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:2429–2436, 2019

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Section: Resultssupporting

confidence: 90%

Acute Changes in NADPH Oxidase 4 in Early Post‐Traumatic Osteoarthritis

Wegner

Campos

Robbins

et al. 2019

Journal Orthopaedic Research

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“…However, the extent to which ROS signalling promotes the establishment of neuronal polarity in vivo remains to be determined. Phenotypes of NADPH oxidase knockout and RNAi knockdown experiments in several experimental animal models suggest that removal of any one NADPH oxidase still allows the nervous systems to form and function remarkably well, at least to a level sufficient for survival under laboratory conditions . This could indicate a degree of functional redundancy.…”

Section: Regulation Of Ros In the Nervous System The Case For The Dementioning

confidence: 99%

Regulation of neuronal development and function by ROS

et al. 2018

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Reactive oxygen species (ROS) have long been studied as destructive agents in the context of nervous system ageing, disease and degeneration. Their roles as signalling molecules under normal physiological conditions is less well understood. Recent studies have provided ample evidence of ROS‐regulating neuronal development and function, from the establishment of neuronal polarity to growth cone pathfinding; from the regulation of connectivity and synaptic transmission to the tuning of neuronal networks. Appreciation of the varied processes that are subject to regulation by ROS might help us understand how changes in ROS metabolism and buffering could progressively impact on neuronal networks with age and disease.

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“…More work will also be needed to further establish the putative causal role of ROS formation for the biology of myeloid leukemia. For example, mouse strains with constitutive or conditional deficiency of NOX enzymes and several regulators are available [85] and may be investigated in transplantation-based or transgenic leukemia models. These studies may help in establishing components in the pathways for ROS formation in cells of myeloid leukemia as candidate drug targets.…”

Section: Future Directionsmentioning

confidence: 99%

NOX-driven ROS formation in cell transformation of FLT3-ITD-positive AML

Jayavelu

Moloney

Böhmer

et al. 2016

Experimental Hematology

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Nox/Duox Family of NADPH Oxidases: Lessons from Knockout Mouse Models

Cited by 113 publications

References 68 publications

Acute Changes in NADPH Oxidase 4 in Early Post‐Traumatic Osteoarthritis

Acute Changes in NADPH Oxidase 4 in Early Post‐Traumatic Osteoarthritis

Regulation of neuronal development and function by ROS

NOX-driven ROS formation in cell transformation of FLT3-ITD-positive AML

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