NOX/NADPH Oxidase, the Superoxide-Generating Enzyme: Its Transcriptional Regulation and Physiological Roles

Katsuyama, Masato

doi:10.1254/jphs.10r01cr

Cited by 95 publications

(76 citation statements)

References 101 publications

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“…In particular, angiotensin II is known to upregulate NADPH oxidase subunits and is commonly upregulated in renal injuries. 30 In addition, it was previously demonstrated that superoxide itself leads to the upregulation of NADPH oxidase in the renal cortex, 31 and that EC-SOD KO mice have increased NADPH activity and subunit expression. 32 The loss of EC-SOD could therefore increase superoxide, leading to a feed-forward mechanism in which NADPH oxidase is further upregulated.…”

Section: Discussionmentioning

confidence: 98%

Extracellular Superoxide Dismutase Protects against Proteinuric Kidney Disease

Tan¹,

Zhou

Lin

et al. 2015

Journal of the American Society of Nephrology

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Extracellular superoxide dismutase (EC-SOD), also known as SOD3, is an antioxidant expressed at high levels in normal adult kidneys. Because oxidative stress contributes to a variety of kidney injuries, we hypothesized that EC-SOD may be protective in CKD progression. To study this hypothesis, we used a murine model of ADR nephropathy characterized by albuminuria and renal dysfunction. We found that levels of EC-SOD diminished throughout the course of disease progression and were associated with increased levels of NADPH oxidase and oxidative stress markers. EC-SOD null mice were sensitized to ADR injury, as evidenced by increases in albuminuria, serum creatinine, histologic damage, and oxidative stress. The absence of EC-SOD led to increased levels of NADPH oxidase and an increase in b-catenin signaling, which has been shown to be pathologic in a variety of kidney injuries. Exposure of EC-SOD null mice to either chronic angiotensin II infusion or to daily albumin injections also caused increased proteinuria. In contrast, EC-SOD null mice subjected to nonproteinuric CKD induced by unilateral ureteral obstruction exhibited no differences compared with wild-type mice. Finally, we also found a decrease in EC-SOD in human CKD biopsy samples, similar to our findings in mice. Therefore, we conclude that EC-SOD is protective in CKDs characterized by proteinuria.

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Section: Discussionmentioning

confidence: 98%

Extracellular Superoxide Dismutase Protects against Proteinuric Kidney Disease

Tan¹,

Zhou

Lin

et al. 2015

Journal of the American Society of Nephrology

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“…The NADPH oxidase subunits; p67 phox , p47 phox , NOXO1, p22 phox , NOX4 and DUOX2 are expressed in NIH3T3 cells [99]. However, only NOX4 and p22 phox have been proven sufficient for generation of ROS [99,102], and are therefore proposed to constitute the volume-sensitive NADPH oxidase in NIH3T3 cells [99], reducing but not excluding a potential role of CK2 regulation of NOX4 though p47 phox in these cells. On the other hand, inhibition of CK2 was demonstrated to increase the production of H 2 O 2 as a result of induced apoptosis [111].…”

Section: Taurine Release Regulation Of the Swelling Induced Signallimentioning

confidence: 99%

“…The effect of LPA and PMA on taurine transport is impaired in the presence of an NADPH oxidase inhibitor [99,101], i.e., PKC and LPA interferes at a step upstream to generation of ROS. NADPH oxidases generates superoxides which are converted by dismutation to the lipid permeable H 2 O 2 se (see [102]). Increased availability of H 2 O 2 leads to activation of tyrosine kinases and reduced phosphatase activity caused by oxidation of the thiol residue at an essential cysteine in the active site [103].…”

Section: Taurine Release Regulation Of the Swelling Induced Signallimentioning

confidence: 99%

Regulation of Taurine Transport Systems by Protein Kinase CK2 in Mammalian Cells

Lambert

Hansen

2011

Cell Physiol Biochem

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Maintaining cell volume is critical for cellular function yet shift in cell volume is a prerequisite for mitosis and apoptosis. The ubiquitously and evolutionary conserved serine/threonine kinase CK2 promotes cell survival and suppresses apoptosis. The present review describes how mammalian cells regulate the cellular content of the major cellular organic osmolyte, taurine with emphasis on CK2 mediated regulation of active taurine uptake and volume-sensitive taurine release. Furthermore, we discuss how CK2-mediated regulation of taurine homeostasis is potentially involved in cellular functions such as proliferation and survival.

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“…NOX4-dependent H 2 O 2 generation seems to be required for myofibroblast differentiation, synthesis of ECM proteins, and contractility mediated by TGF-b1. Moreover, in murine models of lung injury, genetic or pharmacologic targeting of NOX4 attenuated fibrogenesis (3,65,76).…”

Section: Nox4mentioning

confidence: 99%

NOX Modifiers—Just a Step Away from Application in the Therapy of Airway Inflammation?

Wieczfińska

Sokołowska

Pawliczak

2015

Antioxidants & Redox Signaling

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Significance: NADPH oxidase (NOX) enzymes, which are widely expressed in different airway cell types, not only contribute to the maintenance of physiological processes in the airways but also participate in the pathogenesis of many acute and chronic diseases. Therefore, the understanding of NOX isoform regulation, expression, and the manner of their potent inhibition might lead to effective therapeutic approaches. Recent Advances: The study of the role of NADPH oxidases family in airway physiology and pathophysiology should be considered as a work in progress. While key questions still remain unresolved, there is significant progress in terms of our understanding of NOX importance in airway diseases as well as a more efficient way of using NOX modifiers in human settings. Critical Issues: Agents that modify the activity of NADPH enzyme components would be considered useful tools in the treatment of various airway diseases. Nevertheless, profound knowledge of airway pathology, as well as the mechanisms of NOX regulation is needed to develop potent but safe NOX modifiers. Future Directions: Many compounds seem to be promising candidates for development into useful therapeutic agents, but their clinical potential is yet to be demonstrated. Further analysis of basic mechanisms in human settings, high-throughput compound scanning, clinical trials with new and existing molecules, and the development of new drug delivery approaches are the main directions of future studies on NOX modifiers. In this article, we discuss the current knowledge with regard to NOX isoform expression and regulation in airway inflammatory diseases as well as the aptitudes and therapeutic potential of NOX modifiers. Antioxid. Redox Signal. 23,[428][429][430][431][432][433][434][435][436][437][438][439][440][441][442][443][444][445]

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NOX/NADPH Oxidase, the Superoxide-Generating Enzyme: Its Transcriptional Regulation and Physiological Roles

Cited by 95 publications

References 101 publications

Extracellular Superoxide Dismutase Protects against Proteinuric Kidney Disease

Extracellular Superoxide Dismutase Protects against Proteinuric Kidney Disease

Regulation of Taurine Transport Systems by Protein Kinase CK2 in Mammalian Cells

NOX Modifiers—Just a Step Away from Application in the Therapy of Airway Inflammation?

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