ReviewJournal of inherited metabolic disease2012
Mitochondrial ATP synthase: architecture, function and pathology.
Review in Journal of inherited metabolic disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 324 papers, 1 of them a synthesis that pooled it.
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
324 citing papers in PubMed, 1 synthesis or guideline pooled it, 594 citations in OpenAlex.
- A Systematic Review of Proteomics in Obesity: Unpacking the Molecular Puzzle.Current obesity reports · 2024Pooled it
- Article
- Troponin: biology, molecular mechanisms, and multidimensional clinical applications.Molecular biomedicine · 2026Review
- Distinct Urea Cycle Dysfunction Profiles Differentiate Acute Metabolic Decompensation in TMEM70 and MT-ATP6-Related Mitochondrial ATP Synthase Defects.Journal of inherited metabolic disease · 2026Article
- Mitochondrial Complex V Dysfunction in Neurodegeneration: Secondary Bystander or Primary Driver?Brain sciences · 2026Review
- Genetic Diversity and Runs of Homozygosity in Three Masu Salmon (Biomolecules · 2026Article
- Mitochondrial vulnerability to aldehydic load and the role mitochondrial aldehyde dehydrogenases.Pharmacological research · 2026Review
- The mitochondrial protease, LonP1, is a potential cardioprotective target for attenuating doxorubicin-induced cardiomyocyte death.Journal of translational medicine · 2026Article
- Biallelic Loss-Of-Function Variant in ATP5ME Is Associated With Severe and Early Onset Oxidative Phosphorylation Deficiency.Journal of inherited metabolic disease · 2026Article
- Mitophagy in Hepatic Ischemia-Reperfusion Injury: From Mitochondrial Dysfunction to Therapeutic Targeting.Biomolecules · 2026Review
- Mitochondria: The Crossroads of Complement Activation and Kidney Injury Progression.International journal of molecular sciences · 2026Review
- Proteomic signature of the acquired salivary pellicle on zirconia and its role in modulating oral biofilms formation.Odontology · 2026Article
- Developmental Morphokinetics and the Transcriptomic Profile of Bovine First-Cleaved Embryos: Normal vs. Abnormal Divisions.International journal of molecular sciences · 2026Article
- FABP5 confers resistance to drug-induced ROS toxicity in cervical cancer cell lines by suppressing the PPARγ/CPT1A signaling pathway.Discover oncology · 2026Article
- Mitochondrial Dysfunction in Traumatic Brain Injury and Its Theranostic Implications.Biomolecules · 2026Review
- Specific elimination of m.8993T>G mitochondrial haplotype in NARP cybrid cells by CRISPR-Cas9 system.Scientific reports · 2026Article
- MT-ATP6 9035T>C Variant Causes Ataxia With Azoospermia and Apparent Anticipation in a Four-generation Kindred.Cerebellum (London, England) · 2026Observational
- Metabolic Myokines and Adipokines in the Follicular Microenvironment: Implications for Oocyte Competence and IVF Outcomes.International journal of molecular sciences · 2026Review
- Anthelmintic effects of Artemisia herba-alba and Artemisia judaica extracts on Ascaridia galli in poultry.Poultry science · 2026Article
- Spectrum and functions of ion channels and transporters in osteoclasts.Bone research · 2026Review
264 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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human mitochondrial (mt) ATP synthase, or complex V consists of two functional domains: F(1), situated in the mitochondrial matrix, and F(o), located in the inner mitochondrial membrane. Complex V uses the energy created by the proton electrochemical gradient to phosphorylate ADP to ATP. This review covers the architecture, function and assembly of complex V. The role of complex V di-and oligomerization and its relation with mitochondrial morphology is discussed. Finally, pathology related to complex V deficiency and current therapeutic strategies are highlighted. Despite the huge progress in this research field over the past decades, questions remain to be answered regarding the structure of subunits, the function of the rotary nanomotor at a molecular level, and the human complex V assembly process. The elucidation of more nuclear genetic defects will guide physio(patho)logical studies, paving the way for future therapeutic interventions.
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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.