ReviewCell death & disease2011
Mitochondrial complex I and cell death: a semi-automatic shotgun model.
Review in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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
9 citing papers in PubMed.
- The Interplay between Dysregulated Metabolism and Epigenetics in Cancer.Biomolecules · 2023Review
- Nobiletin Exhibits Neuroprotective Effects against Mitochondrial Complex I Inhibition via Regulating Apoptotic Signaling.Experimental neurobiology · 2021Article
- Mitochondrial GWAS and association of nuclear - mitochondrial epistasis with BMI in T1DM patients.BMC medical genomics · 2020Article
- GhMCS1, the Cotton Orthologue of Human GRIM-19, Is a Subunit of Mitochondrial Complex I and Associated with Cotton Fibre Growth.PloS one · 2016Article
- Efficient mitochondrial biogenesis drives incomplete penetrance in Leber's hereditary optic neuropathy.Brain : a journal of neurology · 2014Article
- Metabolic profiling of human CD4+ cells following treatment with methotrexate and anti-TNF-α infliximab.Cell cycle (Georgetown, Tex.) · 2013Article
- Curcumin pretreatment prevents potassium dichromate-induced hepatotoxicity, oxidative stress, decreased respiratory complex I activity, and membrane permeability transition pore opening.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Review
- Rare primary mitochondrial DNA mutations and probable synergistic variants in Leber's hereditary optic neuropathy.PloS one · 2012Article
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.
Funding
Abstract
Mitochondrial dysfunction often leads to cell death and disease. We can now draw correlations between the dysfunction of one of the most important mitochondrial enzymes, NADH:ubiquinone reductase or complex I, and its structural organization thanks to the recent advances in the X-ray structure of its bacterial homologs. The new structural information on bacterial complex I provide essential clues to finally understand how complex I may work. However, the same information remains difficult to interpret for many scientists working on mitochondrial complex I from different angles, especially in the field of cell death. Here, we present a novel way of interpreting the bacterial structural information in accessible terms. On the basis of the analogy to semi-automatic shotguns, we propose a novel functional model that incorporates recent structural information with previous evidence derived from studies on mitochondrial diseases, as well as functional bioenergetics.
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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.