Les NADPH oxydases, Nox

Nguyen, Minh Vu Chuong; Lardy, Bernard; Paclet, Marie-Hélène; Rousset, Francis; Berthier, Sylvie; Baillet, Athan; Grange, Laurent; Gaudin, Philippe; Morel, Françoise

doi:10.1051/medsci/20153101012

Cited by 12 publications

(4 citation statements)

References 45 publications

(61 reference statements)

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“…Nox is a type of oxidative stress enzyme, including Nox1, Nox2, Nox3, Nox4, Nox5, DUox1 and DUox2 9 . Vascular tissue highly expresses Nox1, Nox2, Nox4 and Nox5, of which Nox4 is more expressed in endothelial cells (EC) 10 .…”

Section: Introductionmentioning

confidence: 99%

Mechanism of arterial injury exacerbated by hyperhomocysteinemia in spontaneously hypertensive rats

Zhang

et al. 2023

Sci Rep

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Hypertension associated with hyperhomocysteinemia (HHcy) accounts for 75% of hypertension in China. HHcy plays a synergistic role with hypertension in vascular injury and significantly increases the incidence of cardiovascular and cerebrovascular diseases. The present study aimed to explore the molecular mechanism of HHcy-induced arterial injury in hypertension. Spontaneously hypertensive rats (SHR) were injected intraperitoneally with DL-homocysteine (Hcy) to construct the model of hypertension associated with HHcy (HHcy + SHR). Biological network was employed to identify the material basis of arterial injury in hypertension associated with HHcy. The prediction molecules in oxidative stress and inflammation pathways were experimentally verified by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot (WB) analysis. The HHcy + SHR group significantly increased oxidative stress pathway molecules: nicotinamide adenine dinucleotide phosphate oxidase (Nox); inflammatory pathway molecules: vascular adhesion protein-1 (VAP-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a); as well as inflammatory pathway regulatory factors: nuclear factor-κ-gene binding (NF-κB) p65 and protein kinase B (Akt1). Among them, IL-6 was also significantly increased in the HHcy group. Both oxidative stress and inflammation contributed to the arterial injury of hypertension associated with HHcy, and inflammation mechanism might play a leading role in HHcy aggravating arterial injury, at least partially through the Akt1/NF-κB p65/IL-6 signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Mechanism of arterial injury exacerbated by hyperhomocysteinemia in spontaneously hypertensive rats

Zhang

et al. 2023

Sci Rep

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“…Additionally, the levels of oxidative stress and immune/inflammation are also increased in patients with hypertension ( Guzik and Touyz, 2017 ). It is known that NADPH oxidase (Nox) enzyme is an important member of integrated stress response in the body and is also the main source of ROS ( Cifuentes-Pagano et al, 2012 ; Chuong Nguyen et al, 2015 ). In addition, the Nox family is highly expressed in vascular tissues, among which Nox4 is more expressed in endothelial cells ( Bedard and Krause, 2007 ).…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, in China, folate has been used as an important pharmaceutical ingredient against hypertension combined with HHcy ( Li et al, 2007 ). Besides, folate is also a powerful antioxidant ( Jiang et al, 2010 ) and is closely associated with activated immune cells that highly express folate receptors ( Cifuentes-Pagano et al, 2012 ; Chuong Nguyen et al, 2015 ). However, the precise mechanism underlying folate against arterial injury of hypertension combined with HHcy has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Folate Reverses NF-κB p65/Rela/IL-6 Level Induced by Hyperhomocysteinemia in Spontaneously Hypertensive Rats

Zhang

Xing

et al. 2021

Front. Pharmacol.

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Hyperhomocysteinemia (HHcy) is derived from the abnormal metabolism of homocysteine (Hcy) and is related to metabolic-related diseases. In addition, HHcy combined with hypertension increases the risk of cardiovascular diseases (CVD). However, the mechanism of HHcy aggravating hypertensive arterial damage and the efficacy of folate (FA) as a beneficial supplement have not been fully elucidated. In this study, we established a rat HHcy model and a hypertension combined with HHcy model. Rat tail artery blood pressure (BP), plasma Hcy, serum superoxide dismutase (SOD), and malondialdehyde (MDA) were measured. Rat thoracic aorta was for pathological analysis after 12 weeks of the experiment. The relative expression levels of oxidative stress and immune/inflammation in rat arterial tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. The results demonstrated that the relative expression levels of oxidative stress and immune/inflammation were the highest in the hypertension combined with HHcy group, followed by the hypertension group. Compared with the hypertension group, the hypertension combined with HHcy group up-regulated the expression levels of interleukin-6 (IL-6) and nuclear factor-κ-gene binding (NF-κB) p65/Rela, but not NADPH oxidase (Nox). Furthermore, folate inhibited the expression of IL-6 and NF-κB p65/Rela, reduced the levels of MDA and HHcy, but significantly increased the SOD level. In conclusion, HHcy synergistically aggravated the arterial damage factor of hypertension through immune/inflammatory response. However, folate demonstrated anti-inflammatory properties and reversed the NF-κB p65/Rela/IL-6 level induced by HHcy in hypertensive rats.

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“…The membrane catalytic subunits differentiate the seven isoforms, NOX1 to 5 and two dual oxidases DUOX1 and 2, associated with the membrane protein p22phox with cytosolic regulatory subunits; altogether, they form the NADPH oxidase complexes. [1][2][3][4][5][6] NADPH oxidase substrates are molecular oxygen and the reduced coenzyme NADPH. The catalytic pathway involves electron transfer from cytosolic NADPH to the FAD prosthetic group in the dehydrogenase C-terminal cytosolic domain.…”

Section: Introductionmentioning

confidence: 99%

Development of a caffeic acid–phthalimide hybrid compound for NADPH oxidase inhibition

et al. 2021

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Les NADPH oxydases, Nox

Cited by 12 publications

References 45 publications

Mechanism of arterial injury exacerbated by hyperhomocysteinemia in spontaneously hypertensive rats

Mechanism of arterial injury exacerbated by hyperhomocysteinemia in spontaneously hypertensive rats

Folate Reverses NF-κB p65/Rela/IL-6 Level Induced by Hyperhomocysteinemia in Spontaneously Hypertensive Rats

Development of a caffeic acid–phthalimide hybrid compound for NADPH oxidase inhibition

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