NADPH oxidase-dependent oxidative stress in the failing heart: From pathogenic roles to therapeutic approach

Octavia, Yanti; Rocca, Hans‐Peter Brunner‐La; Moens, An L.

doi:10.1016/j.freeradbiomed.2011.10.482

Cited by 69 publications

(53 citation statements)

References 97 publications

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“…NADPH oxidases (NOXs) have been investigated as a key enzymatic source of ROS and seem to play an important role in the pathogenesis of hypertension, atherosclerosis, and heart failure [72][73][74]. NOXs are multi-subunit transmembrane enzymes that utilize NADPH as an electron donor to reduce oxygen to superoxide anion and hydrogen peroxide.…”

Section: Nadph Oxidases Inhibitorsmentioning

confidence: 99%

Antioxidant Therapies in the Prevention and Treatment of Atrial Fibrillation

Liu¹,

Korantzopoulos²,

Li³

2013

Atrial Fibrillation - Mechanisms and Treatment

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Section: Nadph Oxidases Inhibitorsmentioning

confidence: 99%

Antioxidant Therapies in the Prevention and Treatment of Atrial Fibrillation

Liu¹,

Korantzopoulos²,

Li³

2013

Atrial Fibrillation - Mechanisms and Treatment

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“…There is substantial evidence that systemic and myocardial oxidative stress is augmented during heart failure [12,13]. More recently, increased oxidative stress was also observed in skeletal muscle [14,15,16].…”

Section: Introductionmentioning

confidence: 99%

Influence of N-Acetylcysteine on Oxidative Stress in Slow-Twitch Soleus Muscle of Heart Failure Rats

Martinez

Bonomo

Guizoni

et al. 2015

Cell Physiol Biochem

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Background: Chronic heart failure is characterized by decreased exercise capacity with early exacerbation of fatigue and dyspnea. Intrinsic skeletal muscle abnormalities can play a role in exercise intolerance. Causal or contributing factors responsible for muscle alterations have not been completely defined. This study evaluated skeletal muscle oxidative stress and NADPH oxidase activity in rats with myocardial infarction (MI) induced heart failure. Methods and Results: Four months after MI, rats were assigned to Sham, MI-C (without treatment), and MI-NAC (treated with N-acetylcysteine) groups. Two months later, echocardiogram showed left ventricular dysfunction in MI-C; NAC attenuated diastolic dysfunction. In soleus muscle, glutathione peroxidase and superoxide dismutase activity was decreased in MI-C and unchanged by NAC. 3-nitrotyrosine was similar in MI-C and Sham, and lower in MI-NAC than MI-C. Total reactive oxygen species (ROS) production was assessed by HPLC analysis of dihydroethidium (DHE) oxidation fluorescent products. The 2-hydroxyethidium (EOH)/DHE ratio did not differ between Sham and MI-C and was higher in MI-NAC. The ethidium/DHE ratio was higher in MI-C than Sham and unchanged by NAC. NADPH oxidase activity was similar in Sham and MI-C and lower in MI-NAC. Gene expression of p47^phox was lower in MI-C than Sham. NAC decreased NOX4 and p22^phox expression. Conclusions: We corroborate the case that oxidative stress is increased in skeletal muscle of heart failure rats and show for the first time that oxidative stress is not related to increased NADPH oxidase activity.

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“…Several studies support the hypothesis that inflammation, hyperhomocysteinemia and OS were intimately linked with the pathogenesis of oxidative myocardial damage with consequential IHD 12,13,14 .…”

Section: Introductionmentioning

confidence: 77%

Untitled

2016

IJPSR

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Ischemic heart disease (IHD) is the major cause of morbidmortality in most countries. The involvement of inflammation and oxidative stress (OS) in the development of atherosclerosis, ischemic cardiopathy triggering phenomen, has been investigated. The high sensitive C-reactive protein (hs_CRP) was measured in serum by immunoenzymatic method. Serum total homocysteine (Hcy) concentration was measured by fluorescence polarization immunoessay. Plasma levels of substances reacting with thiobarbituric acid (TBARS) were carried out by fluorimetric method (Yagi). Erythrocyte activity of superoxide dismutase (SOD) and plasma total antioxidant status (TAS) were determined by a colorimetric method at 505nm and 600nm, respectively. Erythrocyte activity of catalase (CAT) was measured by colorimetric assay (Goth). Our study showed significant elevation of hs_CRP, TBARS and Hcy levels in patients compared to controls. While we noted significant decrease in TAS levels, SOD and CAT activities in patients compared to the control group. We also noted positive correlations between: hs_CRP-Hcy, hs_CRP-TBARS, Hcy-TBARS, SOD-TAS, CAT-TAS and negative correlations between: hs_CRP-SOD, hs_CRP-CAT, hs_CRP-TAS, TBARS-SOD, TBARS-CAT, TBARS-TAS, Hcy-SOD, Hcy-CAT and Hcy-TAS. This unsuitability, elevated pro-oxidant rate parameters (Hcy and TBARS) and decrease of antioxidant parameters (SOD, CAT and TAS), is a consequence of inflammation, one of the mechanisms which cause atherogenesis. So our study supports the hypothesis involvement of inflammation and OS in the genesis and progression of atherosclerosis.

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NADPH oxidase-dependent oxidative stress in the failing heart: From pathogenic roles to therapeutic approach

Cited by 69 publications

References 97 publications

Antioxidant Therapies in the Prevention and Treatment of Atrial Fibrillation

Antioxidant Therapies in the Prevention and Treatment of Atrial Fibrillation

Influence of N-Acetylcysteine on Oxidative Stress in Slow-Twitch Soleus Muscle of Heart Failure Rats

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