ArticleThe FEBS journal2011
Modulation of F0F1-ATP synthase activity by cyclophilin D regulates matrix adenine nucleotide levels.
Article in The FEBS journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 47 citations in OpenAlex.
- Proteomic profile of hippocampal growth cones through early postnatal development.Development (Cambridge, England) · 2026Article
- The adenine nucleotide translocase family underlies cardiac ischemia-reperfusion injury through the mitochondrial permeability pore independently of cyclophilin D.Science advances · 2024Article
- Mtfp1 ablation enhances mitochondrial respiration and protects against hepatic steatosis.Nature communications · 2023Article
- Mitochondrial permeability transition pore-dependent necrosis.Journal of molecular and cellular cardiology · 2023Review
- Melatonin-Induced Postconditioning Suppresses NMDA Receptor through Opening of the Mitochondrial Permeability Transition Pore via Melatonin Receptor in Mouse Neurons.International journal of molecular sciences · 2022Article
- Cyclophilin D regulation of the mitochondrial permeability transition pore.Current opinion in physiology · 2022Article
- Regulated cell death in cisplatin-induced AKI: relevance ofAmerican journal of physiology. Renal physiology · 2021Article
- Role of Mitochondrial Calcium and the Permeability Transition Pore in Regulating Cell Death.Circulation research · 2020Review
- Sex Differences in Ischemia/Reperfusion Injury: The Role of Mitochondrial Permeability Transition.Neurochemical research · 2019Review
- Cyclophilin D deficiency attenuates mitochondrial F1Fo ATP synthase dysfunction via OSCP in Alzheimer's disease.Neurobiology of disease · 2019Article
- Cyclophilin D, Somehow a Master Regulator of Mitochondrial Function.Biomolecules · 2018Review
- Estrogen receptor beta modulates permeability transition in brain mitochondria.Biochimica et biophysica acta. Bioenergetics · 2018Article
- Mitochondrial permeability transition in cardiac ischemia-reperfusion: whether cyclophilin D is a viable target for cardioprotection?Cellular and molecular life sciences : CMLS · 2017Review
- Selective Inhibition of the Mitochondrial Permeability Transition Pore Protects against Neurodegeneration in Experimental Multiple Sclerosis.The Journal of biological chemistry · 2016Article
- Molecular mechanisms of cell death: central implication of ATP synthase in mitochondrial permeability transition.Oncogene · 2015Review
- Regulation of mitochondrial ATP synthase in cardiac pathophysiology.American journal of cardiovascular disease · 2015Review
- Role of soluble adenylyl cyclase in mitochondria.Biochimica et biophysica acta · 2014Review
- The mitochondrial permeability transition pore and cancer: molecular mechanisms involved in cell death.Frontiers in oncology · 2014Review
- The C Ring of the F1Fo ATP Synthase Forms the Mitochondrial Permeability Transition Pore: A Critical Appraisal.Frontiers in oncology · 2014Article
- The negative impact of α-ketoglutarate dehydrogenase complex deficiency on matrix substrate-level phosphorylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Cyclophilin D was recently shown to bind to and decrease the activity of F(0)F(1)-ATP synthase in submitochondrial particles and permeabilized mitochondria [Giorgio V et al. (2009) J Biol Chem, 284, 33982-33988]. Cyclophilin D binding decreased both ATP synthesis and hydrolysis rates. In the present study, we reaffirm these findings by demonstrating that, in intact mouse liver mitochondria energized by ATP, the absence of cyclophilin D or the presence of cyclosporin A led to a decrease in the extent of uncoupler-induced depolarization. Accordingly, in substrate-energized mitochondria, an increase in F(0)F(1)-ATP synthase activity mediated by a relief of inhibition by cyclophilin D was evident in the form of slightly increased respiration rates during arsenolysis. However, the modulation of F(0)F(1)-ATP synthase by cyclophilin D did not increase the adenine nucleotide translocase (ANT)-mediated ATP efflux rate in energized mitochondria or the ATP influx rate in de-energized mitochondria. The lack of an effect of cyclophilin D on the ANT-mediated adenine nucleotide exchange rate was attributed to the ∼ 2.2-fold lower flux control coefficient of the F(0)F(1)-ATP synthase than that of ANT, as deduced from measurements of adenine nucleotide flux rates in intact mitochondria. These findings were further supported by a recent kinetic model of the mitochondrial phosphorylation system, suggesting that an ∼ 30% change in F(0)F(1)-ATP synthase activity in fully energized or fully de-energized mitochondria affects the ADP-ATP exchange rate mediated by the ANT in the range 1.38-1.7%. We conclude that, in mitochondria exhibiting intact inner membranes, the absence of cyclophilin D or the inhibition of its binding to F(0)F(1)-ATP synthase by cyclosporin A will affect only matrix adenine nucleotides levels.
Indexed as
Identifiers
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.