ReviewBiochimica et biophysica acta2016
Energy conversion, redox catalysis and generation of reactive oxygen species by respiratory complex I.
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 58 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 133 citations in OpenAlex.
- Fenofibrate alleviates the brain edema after traumatic brain injury by enhancing endothelial OXPHOS.Redox biology · 2026Article
- Targeting the Mitochondrial Phenotype in Cockayne Syndrome Patient Cells: From Bioenergetic Fragility to Pharmacologic Rescue.bioRxiv : the preprint server for biology · 2026Article
- Moonlighting cytosolic function of ACAD9: suppression of TRAF6-mediated osteoclastogenesis and protection against osteoporosis.Cell death & disease · 2026Article
- Lessons, connections, hypotheses and predictions from protein film electrochemistry.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Review
- Serum neuronal, glial and mitochondrial markers in autosomal dominant optic atrophy and Leber hereditary optic neuropathy.Brain communications · 2025Article
- Searching for proton transfer channels in respiratory complex I.Biophysical journal · 2024Article
- Review
- Understanding coenzyme Q.Physiological reviews · 2024Review
- Mitochondrial Physiology of Cellular Redox Regulations.Physiological research · 2024Review
- UPF1 deficiency enhances mitochondrial ROS which promotes an immunosuppressive microenvironment in pancreatic ductal adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mitochondrial Cristae Morphology Reflecting Metabolism, Superoxide Formation, Redox Homeostasis, and Pathology.Antioxidants & redox signaling · 2023Review
- FTSH PROTEASE 3 facilitates Complex I degradation through a direct interaction with the Complex I subunit PSST.The Plant cell · 2023Article
- Using light scattering to assess how phospholipid-protein interactions affect complex I functionality in liposomes.RSC chemical biology · 2023Article
- Reverse electron transfer is activated during aging and contributes to aging and age-related disease.EMBO reports · 2023Article
- Site IQ in mitochondrial complex I generates S1QEL-sensitive superoxide/hydrogen peroxide in both the reverse and forward reactions.The Biochemical journal · 2023Article
- Skeletal muscle mitochondrial interactome remodeling is linked to functional decline in aged female mice.Nature aging · 2023Article
- Single protonation of the reduced quinone in respiratory complex I drives four-proton pumping.FEBS letters · 2023Article
- Metabolic adjustments in response to ATP spilling by the small DX protein in aFrontiers in cell and developmental biology · 2023Article
- Emerging Roles of NDUFS8 Located in Mitochondrial Complex I in Different Diseases.Molecules (Basel, Switzerland) · 2022Review
- Conformational changes in mitochondrial complex I of the thermophilic eukaryoteScience advances · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Complex I (NADH:ubiquinone oxidoreductase) is critical for respiration in mammalian mitochondria. It oxidizes NADH produced by the Krebs' tricarboxylic acid cycle and β-oxidation of fatty acids, reduces ubiquinone, and transports protons to contribute to the proton-motive force across the inner membrane. Complex I is also a significant contributor to cellular oxidative stress. In complex I, NADH oxidation by a flavin mononucleotide, followed by intramolecular electron transfer along a chain of iron-sulfur clusters, delivers electrons and energy to bound ubiquinone. Either at cluster N2 (the terminal cluster in the chain) or upon the binding/reduction/dissociation of ubiquinone/ubiquinol, energy from the redox process is captured to initiate long-range energy transfer through the complex and drive proton translocation. This review focuses on current knowledge of how the redox reaction and proton transfer are coupled, with particular emphasis on the formation and role of semiquinone intermediates in both energy transduction and reactive oxygen species production. This article is part of a Special Issue entitled Respiratory complex I, edited by Volker Zickermann and Ulrich Brandt.
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What OpenQuestion holds
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.