The Role of NOX4 and TRX2 in Angiogenesis and Their Potential Cross-Talk

Chen, Chaofei; Li, Li; Zhou, Huanjiao Jenny; Wang, Min

doi:10.3390/antiox6020042

Cited by 34 publications

(27 citation statements)

References 125 publications

(165 reference statements)

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“…Loss of NOX4 expression was seen in parallel to capillary rarefaction and decreased GSTA1 expression. NOX4 is known to modulate angiogenesis and regulate NRF2 in the heart and vessels [41,42]. On the other hand, NOX4 is believed to be an important source of ROS and oxidative stress in the kidney [1].…”

Section: Discussionmentioning

confidence: 99%

Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution

et al. 2019

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Background NADPH oxidase 4 (NOX4) catalyzes the formation of hydrogen peroxide (H 2 O 2 ). NOX4 is highly expressed in the kidney, but its role in renal injury is unclear and may depend on its specific tissue localization. Methods We performed immunostaining with a specific anti-NOX4 antibody and measured NOX4 mRNA expression in human renal biopsies encompassing diverse renal diseases. We generated transgenic mice specifically overexpressing mouse Nox4 in renal tubular cells and subjected the animals to the unilateral ureteral obstruction (UUO) model of fibrosis. Results In normal human kidney, NOX4 protein expression was at its highest on the basolateral side of proximal tubular cells. NOX4 expression increased in mesangial cells and podocytes in proliferative diabetic nephropathy. In tubular cells, NOX4 protein expression decreased in all types of chronic renal disease studied. This finding was substantiated by decreased NOX4 mRNA expression in the tubulo-interstitial compartment in a repository of 175 human renal biopsies. Overexpression of tubular NOX4 in mice resulted in enhanced renal production of H 2 O 2 , increased NRF2 protein expression and decreased glomerular filtration, likely via stimulation of the tubulo-glomerular feedback. Tubular NOX4 overexpression had no obvious impact on kidney morphology, apoptosis, or fibrosis at baseline. Under acute and chronic tubular injury induced by UUO, overexpression of NOX4 in tubular cells did not modify the course of the disease. Conclusions NOX4 expression was decreased in tubular cells in all types of CKD tested. Tubular NOX4 overexpression did not induce injury in the kidney, and neither modified microvascularization, nor kidney structural lesions in fibrosis.

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Section: Discussionmentioning

confidence: 99%

Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution

et al. 2019

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“…However, high levels of ROS, if global and sustained, evoke mitochondria-dependent neuronal cell death. Therefore, cellular ROS levels are precisely controlled by cellular antioxidant defense mechanisms including catalase, superoxide dismutase [34], and HO-1 [19], and a complex intracellular network of enzymes such as GSH, GSH peroxidase, peroxiredoxin, thioredoxin, and thioredoxin reductase [35]. Nevertheless, imbalance between ROS and antioxidants inside the cells results in mitochondrial dysfunction and neuronal cellular death.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective mechanisms of dieckol against glutamate toxicity through reactive oxygen species scavenging and nuclear factor-like 2/heme oxygenase-1 pathway

Cui

Amarsanaa

Lee

et al. 2019

Korean J Physiol Pharmacol

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Glutamate toxicity-mediated mitochondrial dysfunction and neuronal cell death are involved in the pathogenesis of several neurodegenerative diseases as well as acute brain ischemia/stroke. In this study, we investigated the neuroprotective mechanism of dieckol (DEK), one of the phlorotannins isolated from the marine brown alga Ecklonia cava , against glutamate toxicity. Primary cortical neurons (100 µM, 24 h) and HT22 neurons (5 mM, 12 h) were stimulated with glutamate to induce glutamate toxic condition. The results demonstrated that DEK treatment significantly increased cell viability in a dose-dependent manner (1–50 µM) and recovered morphological deterioration in glutamate-stimulated neurons. In addition, DEK strongly attenuated intracellular reactive oxygen species (ROS) levels, mitochondrial overload of Ca 2+ and ROS, mitochondrial membrane potential (ΔΨ m ) disruption, adenine triphosphate depletion. DEK showed free radical scavenging activity in the cell-free system. Furthermore, DEK enhanced protein expression of heme oxygenase-1 (HO-1), an important anti-oxidant enzyme, via the nuclear translocation of nuclear factor-like 2 (Nrf2). Taken together, we conclude that DEK exerts neuroprotective activities against glutamate toxicity through its direct free radical scavenging property and the Nrf-2/HO-1 pathway activation.

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“…Under certain conditions, various angiogenic factors are produced, and vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors are the key molecular factors. The binding of VEGF/FGF to VEGF receptor (VEGFR)/FGF receptor (FGFR) induces multiple signaling networks, such as mitogen-activated protein kinase (MAPK), phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt), extracellular regulated protein kinase (ERK), and notch pathways, and the signaling cascades result in endothelial cell (EC) survival, proliferation, migration, and tube formation [ 7 – 11 ]. A brief overview of the angiogenesis and the activation pathways is provided in Figure 1 .…”

Section: The Dual Role Of Angiogenesis In Cadmentioning

confidence: 99%

Holistic Regulation of Angiogenesis with Chinese Herbal Medicines as a New Option for Coronary Artery Disease

Yuan

Shi

Xin

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Effectively improving myocardial blood flow and controlling atherosclerotic plaque have always been key and difficult points in the prevention and treatment of coronary artery disease (CAD). Although “therapeutic angiogenesis” is regarded as a promising approach for ischemic heart disease by improving blood flow, angiogenesis itself can induce the destabilization of atherosclerotic plaque, which reflects the double-edged role of angiogenesis. Modulating the balance of angiogenesis can be an important target for CAD treatment. Traditional Chinese medicine (TCM) emphasizes the holistic view and dynamic balance of the body. Furthermore, the principle of activating blood circulation and removing blood stasis (ABCRS) is closely connected with angiogenesis and CAD. Recent research suggests that Chinese herbal medicines for ABCRS are effective in balancing the regulation of angiogenesis. This review presents the progress of recent research on the angiogenesis regulation with Chinese herbal medicines for ABCRS in CAD. Moreover, this review demonstrates that Chinese herbal medicines for ABCRS can not only promote angiogenesis in the ischemic area to improve myocardial blood flow but also alleviate angiogenesis to stabilize plaque in atherosclerosis, which reflects the holistic regulatory role in CAD treatment.

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The Role of NOX4 and TRX2 in Angiogenesis and Their Potential Cross-Talk

Cited by 34 publications

References 125 publications

Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution

Tubular NOX4 expression decreases in chronic kidney disease but does not modify fibrosis evolution

Neuroprotective mechanisms of dieckol against glutamate toxicity through reactive oxygen species scavenging and nuclear factor-like 2/heme oxygenase-1 pathway

Holistic Regulation of Angiogenesis with Chinese Herbal Medicines as a New Option for Coronary Artery Disease

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