ArticleThe Journal of biological chemistry2009
Lack of oxygen deactivates mitochondrial complex I: implications for ischemic injury?
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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Who cites it
68 citing papers in PubMed, 126 citations in OpenAlex.
- Mitochondrial genome ofFrontiers in plant science · 2026Article
- The Role of Machine Perfusion for Liver Transplantation in Children.Pediatric transplantation · 2025Review
- Dysfunctional Electron Transport Chain Assembly in COXPD8.Journal of cardiovascular development and disease · 2025Article
- Therapeutic strategies to ameliorate mitochondrial oxidative stress in ischaemia-reperfusion injury: A narrative review.Clinical science (London, England : 1979) · 2025Review
- Potential for flexible lactate shuttling between astrocytes and neurons to mitigate against diving-induced hypoxia.Frontiers in neuroanatomy · 2025Article
- Residual Complex I activity and amphidirectional Complex II operation support glutamate catabolism through mtSLP in anoxia.Scientific reports · 2024Article
- Phospholipids can regulate complex I assembly independent of their role in maintaining mitochondrial membrane integrity.Cell reports · 2023Article
- Transgenic NADH dehydrogenase restores oxygen regulation of breathing in mitochondrial complex I-deficient mice.Nature communications · 2023Article
- Cryo-EM structures define ubiquinone-10 binding to mitochondrial complex I and conformational transitions accompanying Q-site occupancy.Nature communications · 2022Article
- The coupling mechanism of mammalian mitochondrial complex I.Nature structural & molecular biology · 2022Article
- Genome-wide CRISPR/Cas9 deletion screen defines mitochondrial gene essentiality and identifies routes for tumour cell viability in hypoxia.Communications biology · 2021Article
- Mitochondria and Pharmacologic Cardiac Conditioning-At the Heart of Ischemic Injury.International journal of molecular sciences · 2021Review
- Biphasic effect of metformin on human cardiac energetics.Translational research : the journal of laboratory and clinical medicine · 2021Article
- Inhibition of mitochondrial and cytosolic calpain attenuates atrophy in myotubes co-cultured with colon carcinoma cells.Oncology letters · 2021Article
- Proteomic analysis reveals ginsenoside Rb1 attenuates myocardial ischemia/reperfusion injury through inhibiting ROS production from mitochondrial complex I.Theranostics · 2021Article
- Nitric Oxide in Macrophage Immunometabolism: Hiding in Plain Sight.Metabolites · 2020Review
- Comparison of Effects of Metformin, Phenformin, and Inhibitors of Mitochondrial Complex I on Mitochondrial Permeability Transition and Ischemic Brain Injury.Biomolecules · 2020Article
- The new role of FExperimental neurology · 2020Review
- Chronic heart failure with diabetes mellitus is characterized by a severe skeletal muscle pathology.Journal of cachexia, sarcopenia and muscle · 2020Article
- 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
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
For S-nitrosothiols and peroxynitrite to interfere with the activity of mitochondrial complex I, prior transition of the enzyme from its active (A) to its deactive, dormant (D) state is necessary. We now demonstrate accumulation of the D-form of complex I in human epithelial kidney cells after prolonged hypoxia. Upon reoxygenation after hypoxia there was an initial delay in the return of the respiration rate to normal. This was due to the accumulation of the D-form and its slow, substrate-dependent reconversion to the A-form. Reconversion to the A-form could be prevented by prolonged incubation with endogenously generated NO. We propose that the hypoxic transition from the A-form to the D-form of complex I may be protective, because it would act to reduce the electron burst and the formation of free radicals during reoxygenation. However, this may become an early pathophysiological event when NO-dependent formation of S-nitrosothiols or peroxynitrite structurally modifies complex I in its D-form and impedes its return to the active state. These observations provide a mechanism to account for the severe cell injury that follows hypoxia and reoxygenation when accompanied by NO generation.
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Registered trials
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.