ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Nox2 as a potential target of mitochondrial superoxide and its role in endothelial oxidative stress.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Chronic mitochondria antioxidant treatment in older adults alters the circulating milieu to improve endothelial cell function and mitochondrial oxidative stress.American journal of physiology. Heart and circulatory physiology · 2023Trial
- SK3 channel and mitochondrial ROS mediate NADPH oxidase-independent NETosis induced by calcium influx.Proceedings of the National Academy of Sciences of the United States of America · 2015Trial
- Sex-dependent differences in mitochondrial protein acetylation in metabolic condition, oxidative stress, vascular dysfunction, hypertension, and cardiovascular disease.Clinical science (London, England : 1979) · 2026Review
- Electrostatic lipidopathy drives human diabetic heart failure.Cardiovascular diabetology. Endocrinology reports · 2026Article
- NOX2 Contributes to High-Frequency Outer Hair Cell Vulnerability in the Cochlea.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- Modulation of NOX2 causes obesity-mediated atrial fibrillation.The Journal of clinical investigation · 2024Article
- Deacetylation mimetic mutation of mitochondrial SOD2 attenuates ANG II-induced hypertension by protecting against oxidative stress and inflammation.American journal of physiology. Heart and circulatory physiology · 2024Article
- Review
- Pitfalls of Mitochondrial Redox Signaling Research.Antioxidants (Basel, Switzerland) · 2023Review
- Effects of ROS pathway inhibitors and NADH and FADHArchives of biochemistry and biophysics · 2023Article
- Mitochondrial Oxidative Stress and Mitophagy Activation Contribute to TNF-Dependent Impairment of Myogenesis.Antioxidants (Basel, Switzerland) · 2023Article
- Coupling of phagocytic NADPH oxidase activity and mitochondrial superoxide production.Frontiers in cardiovascular medicine · 2022Article
- Oxidative Stress in Preterm Newborns.Antioxidants (Basel, Switzerland) · 2021Review
- Avocado Oil Prevents Kidney Injury and Normalizes Renal Vasodilation after Adrenergic Stimulation in Hypertensive Rats: Probable Role of Improvement in Mitochondrial Dysfunction and Oxidative Stress.Life (Basel, Switzerland) · 2021Article
- Metabolic Pathways Involved in Formation of Spontaneous and Lipopolysaccharide-Induced Neutrophil Extracellular Traps (NETs) Differ in Obesity and Systemic Inflammation.International journal of molecular sciences · 2021Article
- Differential ROS-Mediated Phosphorylation of Drp1 in Mitochondrial Fragmentation Induced by Distinct Cell Death Conditions in Cerebellar Granule Neurons.Oxidative medicine and cellular longevity · 2021Article
- Is Oxidative Stress the Link Between Cerebral Small Vessel Disease, Sleep Disruption, and Oligodendrocyte Dysfunction in the Onset of Alzheimer's Disease?Frontiers in physiology · 2021Review
- Mitochondria Are Potential Targets for the Development of New Drugs Against Neutrophilic Inflammation in Severe Pneumonia Including COVID-19.Frontiers in pharmacology · 2021Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Superoxide (O2(·-)) production by the NADPH oxidases is implicated in the pathogenesis of many cardiovascular diseases, including hypertension. We have previously shown that activation of NADPH oxidases increases mitochondrial O2(·-) which is inhibited by the ATP-sensitive K(+) channel (mitoKATP) inhibitor 5-hydroxydecanoic acid and that scavenging of mitochondrial or cytoplasmic O2(·-) inhibits hypertension. We hypothesized that mitoKATP-mediated mitochondrial O2(·-) potentiates cytoplasmic O2(·-) by stimulation of NADPH oxidases. In this work we studied Nox isoforms as a potential target of mitochondrial O2(·-). We tested contribution of reverse electron transfer (RET) from complex II to complex I in mitochondrial O2(·-) production and NADPH oxidase activation in human aortic endothelial cells. Activation of mitoKATP with low dose of diazoxide (100 nM) decreased mitochondrial membrane potential (tetramethylrhodamine methyl ester probe) and increased production of mitochondrial and cytoplasmic O2(·-) measured by site-specific probes and mitoSOX. Inhibition of RET with complex II inhibitor (malonate) or complex I inhibitor (rotenone) attenuated the production of mitochondrial and cytoplasmic O2(·-). Supplementation with a mitochondria-targeted SOD mimetic (mitoTEMPO) or a mitochondria-targeted glutathione peroxidase mimetic (mitoEbselen) inhibited production of mitochondrial and cytoplasmic O2(·-). Inhibition of Nox2 (gp91ds) or Nox2 depletion with small interfering RNA but not Nox1, Nox4, or Nox5 abolished diazoxide-induced O2(·-) production in the cytoplasm. Treatment of angiotensin II-infused mice with RET inhibitor dihydroethidium (malate) significantly reduced blood pressure. Our study suggests that mitoKATP-mediated mitochondrial O2(·-) stimulates cytoplasmic Nox2, contributing to the development of endothelial oxidative stress and hypertension.
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Registered trials
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