ArticleCirculation research2011
Redox regulation of mitochondrial ATP synthase: implications for cardiac resynchronization therapy.
Article in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 158 citations in OpenAlex.
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- Impacts of Cardiac Dyssynchrony and Resynchronisation on Cellular Metabolism and Mitochondria: Current Understanding for Future Applications.Arrhythmia & electrophysiology review · 2026Review
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
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- Concepts of Cardiac Dyssynchrony and Dynamic Approach.Diagnostics (Basel, Switzerland) · 2024Review
- The Role of Protein S-Nitrosylation in Mitochondrial Quality Control in Central Nervous System Diseases.Aging and disease · 2024Review
- Cold Atmospheric Plasma: Possible Cure of Autoimmune Disorders and Cancer via Attenuating Inflammation.International journal of biological sciences · 2024Review
- Redox dynamics in seeds ofFrontiers in plant science · 2024Article
- Targeting Mitochondrial Metabolism to Save the Failing Heart.Life (Basel, Switzerland) · 2023Review
- Prevalence of Hypertension and Obesity: Profile of Mitochondrial Function and Markers of Inflammation and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Article
- Regulation of Mitochondrial Hydrogen Peroxide Availability by Protein S-glutathionylation.Cells · 2022Review
- Conditions Conducive to the Glutathionylation of Complex I Subunit NDUFS1 Augment ROS Production following the Oxidation of Ubiquinone Linked Substrates, Glycerol-3-Phosphate and Proline.Antioxidants (Basel, Switzerland) · 2022Article
- The multiple facets of mitochondrial regulations controlling cellular thermogenesis.Cellular and molecular life sciences : CMLS · 2022Review
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- Protective effects of cardiac resynchronization therapy in a canine model with experimental heart failure by improving mitochondrial function: a mitochondrial proteomics study.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2021Article
- Pharmacological Inhibition of S-Nitrosoglutathione Reductase Reduces Cardiac Damage Induced by Ischemia-Reperfusion.Antioxidants (Basel, Switzerland) · 2021Article
- Protein S-nitrosation differentially modulates tomato responses to infection by hemi-biotrophic oomycetes of Phytophthora spp.Horticulture research · 2021Article
- The redox language in neurodegenerative diseases: oxidative post-translational modifications by hydrogen peroxide.Cell death & disease · 2021Review
- The Effect of Acute Aerobic Exercise on Redox Homeostasis and Mitochondrial Function of Rat White Adipose Tissue.Oxidative medicine and cellular longevity · 2021Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleCardiac resynchronization therapy (CRT) is an effective clinical treatment for heart failure patients with conduction delay, impaired contraction, and energetics. Our recent studies have revealed that mitochondrial posttranslational modifications (PTM) may contribute to its benefits, motivating the present study of the oxidative regulation of mitochondrial ATP synthase.
objectivesWe tested whether CRT alteration of ATP synthase function is linked to cysteine (Cys) oxidative PTM (Ox-PTM) of specific ATP synthase subunits. METHODS AND
resultsCanine left ventricular myocardium was collected under conditions to preserve Ox-PTM from control, dyssynchronous heart failure (DHF), or hearts that had undergone CRT. In-gel ATPase activity showed that CRT increased ATPase activity by approximately 2-fold (P<0.05) over DHF, approaching control levels, and this effect was recapitulated with a reducing agent. ATP synthase function and 3 Ox-PTM: disulfide bond, S-glutathionylation and S-nitrosation were assessed. ATP synthase from DHF hearts contained 2 novel disulfide bonds, between ATP synthase α subunits themselves and between α and γ subunits, both of which were decreased in CRT hearts (4.38 ± 0.13- and 4.23 ± 0.36-fold, respectively, P<0.01). S-glutathionylation of ATP synthase α subunit occurred in DHF hearts and was decreased by CRT (1.56 ± 0.16-fold, P<0.04). In contrast, S-nitrosation of ATP synthase α subunit in DHF hearts was lower than in CRT hearts (1.53 ± 0.19-fold, P<0.05). All modifications occurred at ATP synthase α subunit Cys294 and Cys to Ser mutation indicated that this residue is critical for ATP synthase function.
conclusionsA selective Cys in ATP synthase α subunit is targeted by multiple Ox-PTM suggesting that this Cys residue may act as a redox sensor modulating ATP synthase function.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.