ReviewBiochimica et biophysica acta2016
Ischemic A/D transition of mitochondrial complex I and its role in ROS generation.
Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 140 citations in OpenAlex.
- Mitochondrial complex I as a master regulator of redox signaling: From structural architecture to directionality of electron transport.Free radical biology & medicine · 2026Review
- Article
- An endothelial RNA splicing atlas catalogs effects of IL-1β and identifies an alternative PROCR isoform with genetic links to pleiotropic vascular disease.American journal of human genetics · 2026Article
- Chlamydia trachomatis disrupts host metabolism in primary cervical epithelial cells.World journal of microbiology & biotechnology · 2025Article
- Global conformations ofScience advances · 2025Article
- Rescuing Ischemic Brain Injury by Rewiring Mitochondrial Electron Flow.bioRxiv : the preprint server for biology · 2025Article
- Dysfunctional Electron Transport Chain Assembly in COXPD8.Journal of cardiovascular development and disease · 2025Article
- Gene therapy prevents onset of mitochondrial cardiomyopathy in neonatal mice with Ndufs6 deficiency.Cell death discovery · 2025Article
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- Mitochondrial complex-1 as a therapeutic target for cardiac diseases.Molecular and cellular biochemistry · 2025Review
- Altered mitochondria-associated ER membrane (MAM) function shifts mitochondrial metabolism in amyotrophic lateral sclerosis (ALS).Nature communications · 2025Article
- Potential for flexible lactate shuttling between astrocytes and neurons to mitigate against diving-induced hypoxia.Frontiers in neuroanatomy · 2025Article
- The Influence of Oxidative Stress Markers in Patients with Ischemic Stroke.Biomolecules · 2024Review
- Mitochondrial responses to constant and cyclic hypoxia depend on the oxidized fuel in a hypoxia-tolerant marine bivalve Crassostrea gigas.Scientific reports · 2024Article
- Residual Complex I activity and amphidirectional Complex II operation support glutamate catabolism through mtSLP in anoxia.Scientific reports · 2024Article
- Utilizing reactive oxygen species-scavenging nanoparticles for targeting oxidative stress in the treatment of ischemic stroke: A review.Open medicine (Warsaw, Poland) · 2024Review
- Disorders of Endogenous and Exogenous Antioxidants in Neurological Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Preventing mitochondrial reverse electron transport as a strategy for cardioprotection.Basic research in cardiology · 2023Review
- Mechanism of rotenone binding to respiratory complex I depends on ligand flexibility.Scientific reports · 2023Article
- Reverse Electron Transport at Mitochondrial Complex I in Ischemic Stroke, Aging, and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
5 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
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Mitochondrial complex I (NADH:ubiquinone oxidoreductase) is a key enzyme in cellular energy metabolism and provides approximately 40% of the proton-motive force that is utilized during mitochondrial ATP production. The dysregulation of complex I function--either genetically, pharmacologically, or metabolically induced--has severe pathophysiological consequences that often involve an imbalance in the production of reactive oxygen species (ROS). Slow transition of the active (A) enzyme to the deactive, dormant (D) form takes place during ischemia in metabolically active organs such as the heart and brain. The reactivation of complex I occurs upon reoxygenation of ischemic tissue, a process that is usually accompanied by an increase in cellular ROS production. Complex I in the D-form serves as a protective mechanism preventing the oxidative burst upon reperfusion. Conversely, however, the D-form is more vulnerable to oxidative/nitrosative damage. Understanding the so-called active/deactive (A/D) transition may contribute to the development of new therapeutic interventions for conditions like stroke, cardiac infarction, and other ischemia-associated pathologies. In this review, we summarize current knowledge on the mechanism of A/D transition of mitochondrial complex I considering recently available structural data and site-specific labeling experiments. In addition, this review discusses in detail the impact of the A/D transition on ROS production by complex I and the S-nitrosation of a critical cysteine residue of subunit ND3 as a strategy to prevent oxidative damage and tissue damage during ischemia-reperfusion injury. This article is part of a Special Issue entitled Respiratory complex I, edited by Volker Zickermann and Ulrich Brandt.
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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.