ArticleAntioxidants & redox signaling2013
Conformational change of mitochondrial complex I increases ROS sensitivity during ischemia.
Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 79 citations in OpenAlex.
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- Hypoxic preconditioning increases mitochondrial respiration and HFrontiers in molecular neuroscience · 2025Article
- Proton-Translocating NADH-Ubiquinone Oxidoreductase: Interaction with Artificial Electron Acceptors, Inhibitors, and Potential Medicines.International journal of molecular sciences · 2024Review
- Progress in the Study of Chemical Structure and Pharmacological Effects of Total Paeony Glycosides Isolated fromCurrent issues in molecular biology · 2024Review
- Preventing mitochondrial reverse electron transport as a strategy for cardioprotection.Basic research in cardiology · 2023Review
- A New Quinone-Based Inhibitor of Mitochondrial Complex I in D-Conformation, Producing Invasion Reduction and Sensitization to Venetoclax in Breast Cancer Cells.Antioxidants (Basel, Switzerland) · 2023Article
- ND3 Cys39 in complex I is exposed during mitochondrial respiration.Cell chemical biology · 2022Article
- Mitochondrial redox regulation and myocardial ischemia-reperfusion injury.American journal of physiology. Cell physiology · 2022Review
- BYHW Decoction Improves Cognitive Impairments in Rats with Cerebral Microinfarcts via Activation of the PKA/CREB Pathway.Oxidative medicine and cellular longevity · 2022Article
- Reduction in hypoxia-reoxygenation-induced myocardial mitochondrial damage with exogenous methane.Journal of cellular and molecular medicine · 2021Article
- Mitochondria as a therapeutic target for cardiac ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2021Review
- Structural basis for a complex I mutation that blocks pathological ROS production.Nature communications · 2021Article
- Bioactivity of Inhaled Methane and Interactions With Other Biological Gases.Frontiers in cell and developmental biology · 2021Review
- Suppression of Superoxide-Hydrogen Peroxide Production at Site IQ of Mitochondrial Complex I Attenuates Myocardial Stunning and Improves Postcardiac Arrest Outcomes.Critical care medicine · 2020Article
- Attenuation of Equine Lentivirus Alters Mitochondrial Protein Expression Profile from Inflammation to Apoptosis.Journal of virology · 2019Article
- Brain Ischemia/Reperfusion Injury and Mitochondrial Complex I Damage.Biochemistry. Biokhimiia · 2019Review
- Inhibition of the ubiquitous calpains protects complex I activity and enables improved mitophagy in the heart following ischemia-reperfusion.American journal of physiology. Cell physiology · 2019Article
- Response by Dunham-Snary and Archer to Letter Regarding Article, "Ndufs2, a Core Subunit of Mitochondrial Complex I, Is Essential for Acute Oxygen-Sensing and Hypoxic Pulmonary Vasoconstriction".Circulation research · 2019Article
- Deactivation of mitochondrial complex I after hypoxia-ischemia in the immature brain.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Physiologic Implications of Reactive Oxygen Species Production by Mitochondrial Complex I Reverse Electron Transport.Antioxidants (Basel, Switzerland) · 2019Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimsMyocardial ischemia/reperfusion (I/R) is associated with mitochondrial dysfunction and subsequent cardiomyocyte death. The generation of excessive quantities of reactive oxygen species (ROS) and resultant damage to mitochondrial enzymes is considered an important mechanism underlying reperfusion injury. Mitochondrial complex I can exist in two interconvertible states: active (A) and deactive or dormant (D). We have studied the active/deactive (A/D) equilibrium in several tissues under ischemic conditions in vivo and investigated the sensitivity of both forms of the heart enzyme to ROS.
resultsWe found that in the heart, t½ of complex I deactivation during ischemia was 10 min, and that reperfusion resulted in the return of A/D equilibrium to its initial level. The rate of superoxide generation by complex I was higher in ischemic samples where content of the D-form was higher. Only the D-form was susceptible to inhibition by H2O2 or superoxide, whereas turnover-dependent activation of the enzyme resulted in formation of the A-form, which was much less sensitive to ROS. The mitochondrial-encoded subunit ND3, most likely responsible for the sensitivity of the D-form to ROS, was identified by redox difference gel electrophoresis. INNOVATION: A combined in vivo and biochemical approach suggests that sensitivity of the mitochondrial system to ROS during myocardial I/R can be significantly affected by the conformational state of complex I, which may therefore represent a new therapeutic target in this setting.
conclusionThe presented data suggest that transition of complex I into the D-form in the absence of oxygen may represent a key event in promoting cardiac injury during I/R.
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