ReviewLife (Basel, Switzerland)2021
The ATP Synthase Deficiency in Human Diseases.
Review in Life (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Variability of Clinical Phenotypes Caused by Isolated Defects of Mitochondrial ATP Synthase.Physiological research · 2024Pooled it
- The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Mitochondrial Complex V Dysfunction in Neurodegeneration: Secondary Bystander or Primary Driver?Brain sciences · 2026Review
- Investigating the relationship between ATP synthase and the TCA cycle by crosslinking mass spectrometry.Nature communications · 2026Article
- ATP5A1 succinylation as a key driver for the transition of myocardial ischemia to development of heart failure.Basic research in cardiology · 2026Article
- Exploring new benefits of vitamin A: alleviating hypoxia-induced mitochondrial stress and mitophagy in the gills of adult grass carp (Ctenopharyngodon idellus).Journal of animal science and biotechnology · 2025Article
- Metabolic costs and trade-offs of hypermetabolism in human motor neurons with ATP synthase deficiency.Communications biology · 2025Article
- Mitochondrial ATP synthase 8 single-nucleotide polymorphism affects oxidative stress and survival of mice.Pflugers Archiv : European journal of physiology · 2025Article
- Dominant negative ATP5F1A variants disrupt oxidative phosphorylation causing neurological disorders.EMBO molecular medicine · 2025Article
- Molecular machineries shaping the mitochondrial inner membrane.Nature reviews. Molecular cell biology · 2025Review
- Astaxanthin Alleviates Oxidative Stress in Mouse Preantral Follicles and Enhances Follicular Development Through the AMPK Signaling Pathway.International journal of molecular sciences · 2025Article
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- Calcium signaling in postsynaptic mitochondria: mechanisms, dynamics, and role in ATP production.Frontiers in molecular neuroscience · 2025Review
- Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.Frontiers in neuroscience · 2025Review
- Metformin attenuates high-carbohydrate diet-induced redox imbalance, inflammation, and mitochondrial dysfunction in Megalobrama amblycephala.Fish physiology and biochemistry · 2024Article
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- Peptides Targeting the IF1-ATP Synthase Complex Modulate the Permeability Transition Pore in Cancer HeLa Cells.International journal of molecular sciences · 2024Article
- An adenosine derivative promotes mitochondrial supercomplexes reorganization and restoration of mitochondria structure and bioenergetics in a diethylnitrosamine-induced hepatocellular carcinoma model.Scientific reports · 2024Article
- Variants in Human ATP Synthase Mitochondrial Genes: Biochemical Dysfunctions, Associated Diseases, and Therapies.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Human diseases range from gene-associated to gene-non-associated disorders, including age-related diseases, neurodegenerative, neuromuscular, cardiovascular, diabetic diseases, neurocognitive disorders and cancer. Mitochondria participate to the cascades of pathogenic events leading to the onset and progression of these diseases independently of their association to mutations of genes encoding mitochondrial protein. Under physiological conditions, the mitochondrial ATP synthase provides the most energy of the cell via the oxidative phosphorylation. Alterations of oxidative phosphorylation mainly affect the tissues characterized by a high-energy metabolism, such as nervous, cardiac and skeletal muscle tissues. In this review, we focus on human diseases caused by altered expressions of ATP synthase genes of both mitochondrial and nuclear origin. Moreover, we describe the contribution of ATP synthase to the pathophysiological mechanisms of other human diseases such as cardiovascular, neurodegenerative diseases or neurocognitive disorders.
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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.