Structure and mechanisms of ROS generation by NADPH oxidases

Magnani, Francesca; Mattevi, Andrea

doi:10.1016/j.sbi.2019.03.001

Cited by 141 publications

(97 citation statements)

References 51 publications

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“…The different isoforms of NOX contain homologs of the NOX2 gp91-phox subunit. Structural homology of the catalytic core is preserved within NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2, however regulation, localization and function slightly vary across isoforms (93).…”

Section: Vascular Nadph Oxidase (Nox)mentioning

confidence: 99%

Reactive Oxygen Species (ROS), Intimal Thickening, and Subclinical Atherosclerotic Disease

Burtenshaw

Kitching

Redmond

et al. 2019

Front. Cardiovasc. Med.

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Arteriosclerosis causes significant morbidity and mortality worldwide. Central to this process is the development of subclinical non-atherosclerotic intimal lesions before the appearance of pathologic intimal thickening and advanced atherosclerotic plaques. Intimal thickening is associated with several risk factors, including oxidative stress due to reactive oxygen species (ROS), inflammatory cytokines and lipid. The main ROS producing systems in-vivo are reduced nicotinamide dinucleotide phosphate (NADPH) oxidase (NOX). ROS effects are context specific. Exogenous ROS induces apoptosis and senescence, whereas intracellular ROS promotes stem cell differentiation, proliferation, and migration. Lineage tracing studies using murine models of subclinical atherosclerosis have revealed the contributory role of medial smooth muscle cells (SMCs), resident vascular stem cells, circulating bone-marrow progenitors and endothelial cells that undergo endothelial-mesenchymal-transition (EndMT). This review will address the putative physiological and patho-physiological roles of ROS in controlling vascular cell fate and ROS contribution to vascular regeneration and disease progression.

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Section: Vascular Nadph Oxidase (Nox)mentioning

confidence: 99%

Reactive Oxygen Species (ROS), Intimal Thickening, and Subclinical Atherosclerotic Disease

Burtenshaw

Kitching

Redmond

et al. 2019

Front. Cardiovasc. Med.

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“…The transmembrane enzymes, NADPH oxidases (NOXs), are considered the main source of intracellular ROS in various cell types [ 16 , 17 ]. Interestingly, the functional interaction between NOXs and TRPVs has been implicated in various pathophysiological conditions [ 18 , 19 , 20 ].…”

Section: Resultsmentioning

confidence: 99%

“…Several anti-cancer agents stimulate apoptosis via ROS production in human ovarian cancer cells [ 50 , 51 ]. In response to physiological and pharmacological stimuli, ROS can be produced by oxidases such as NADPH oxidases (NOXs), which are considered the main source of ROS in cells [ 16 , 17 ]. NOXs are expressed in human cancer cell lines with functions in cell proliferation and tumorigenesis [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

TRPV1 Antagonist DWP05195 Induces ER Stress-Dependent Apoptosis through the ROS-p38-CHOP Pathway in Human Ovarian Cancer Cells

Wang

Lee

Lim

et al. 2020

Cancers

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In addition to their analgesic activity, transient receptor potential vanilloid 1 (TRPV1) agonists and antagonists demonstrate profound anti-cancer activities in various human cancers. In the present study, we investigated the anti-cancer activity of a novel TRPV1 antagonist, DWP05195, and evaluated its molecular mechanism in human ovarian cancer cells. DWP05195 demonstrated potent growth inhibitory effects in all five ovarian cancer cell lines examined. DWP05195 induced apoptosis through the activation of caspase-3, -8, and -9. DWP05195 induced C/EBP homologous protein (CHOP) expression and endoplasmic reticulum (ER) stress. Sodium phenylbutyrate (4-PBA), an ER-stress inhibitor, and CHOP knockdown significantly suppressed DWP5195-induced cell death. DWP05195-enhanced CHOP expression stimulated intrinsic and extrinsic apoptotic pathways through the regulation of Bcl2-like11 (BIM), death receptor 4 (DR4), and DR5. DWP05195-induced cell death was associated with increased reactive oxygen species (ROS) levels and p38 pathway activation. Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation. Inhibition of NADPH oxidase (NOX) through p47phox knockdown abolished DWP05195-induced CHOP expression and cell death. Taken together, the findings indicate that DWP05195 induces ER stress-induced apoptosis via the ROS-p38-CHOP pathway in human ovarian cancer cells.

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“…The five family members (NOX 1-5) share the same structural characteristics, including a common catalytic core composed of two domains: the dehydrogenase domain and the transmembrane domain that ensures membrane localization of these enzymes. Electrons are transferred from cytosolic NADPH to FAD located in the dehydrogenase domain, then to the inner and outer heme present in the transmembrane domain, and finally to oxygen located on the opposite site of the membrane, thus generating either superoxide (NOX 1-3, NOX 5) or H 2 O 2 (NOX 4) (reviewed in [17]). NOXs are implicated in CVD pathologies, including myocardial ischemia-reperfusion injuries, myocardial damage, and cardiomyocyte death [18,19].…”

Section: Ros Ros Sources and Sitesmentioning

confidence: 99%

Effects of Oxidative Stress on Protein Translation: Implications for Cardiovascular Diseases

Ghosh

Shcherbik

2020

IJMS

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Cardiovascular diseases (CVDs) are a group of disorders that affect the heart and blood vessels. Due to their multifactorial nature and wide variation, CVDs are the leading cause of death worldwide. Understanding the molecular alterations leading to the development of heart and vessel pathologies is crucial for successfully treating and preventing CVDs. One of the causative factors of CVD etiology and progression is acute oxidative stress, a toxic condition characterized by elevated intracellular levels of reactive oxygen species (ROS). Left unabated, ROS can damage virtually any cellular component and affect essential biological processes, including protein synthesis. Defective or insufficient protein translation results in production of faulty protein products and disturbances of protein homeostasis, thus promoting pathologies. The relationships between translational dysregulation, ROS, and cardiovascular disorders will be examined in this review.

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Structure and mechanisms of ROS generation by NADPH oxidases

Cited by 141 publications

References 51 publications

Reactive Oxygen Species (ROS), Intimal Thickening, and Subclinical Atherosclerotic Disease

Reactive Oxygen Species (ROS), Intimal Thickening, and Subclinical Atherosclerotic Disease

TRPV1 Antagonist DWP05195 Induces ER Stress-Dependent Apoptosis through the ROS-p38-CHOP Pathway in Human Ovarian Cancer Cells

Effects of Oxidative Stress on Protein Translation: Implications for Cardiovascular Diseases

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