ArticlePLoS biology2021
Generation of mitochondrial reactive oxygen species is controlled by ATPase inhibitory factor 1 and regulates cognition.
Article in PLoS biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- ATPIF1, the rheostat in mitochondrial bioenergetics and dysfunction in diseases.Mitochondrion · 2026Review
- Mitochondrial Permeability Transition Regulators As Emerging Therapeutic Targets in Aging and Neurodegeneration: Recent Insights.Journal of molecular neuroscience : MN · 2026Review
- Immunohistochemical Markers of Mitochondrial Electron Transport Chain Instability in Human Brain Regions: A Study of Aging and Alzheimer's Disease.International journal of molecular sciences · 2026Article
- Strategic Targeting of Mitochondria: Bridging Biology and Therapy for Health Benefits.Cell biochemistry and biophysics · 2026Review
- The critical role of Atpif1 in Her2-targeted CAR-T cell therapy for solid tumor via modulation of metabolism and mtDNA-STING signal pathway.Frontiers in immunology · 2026Article
- NMR assignments of the human homodimeric mitochondrial ATP synthase inhibitor IF1.Biomolecular NMR assignments · 2025Article
- NMR assignments of the human homodimeric mitochondrial ATP synthase inhibitor IF1.Research square · 2025Article
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.PLoS biology · 2025Article
- Mitochondrial Complex I and ROS control neuromuscular function through opposing pre- and postsynaptic mechanisms.bioRxiv : the preprint server for biology · 2025Article
- Refinement of a workflow for human relevance assessment of adverse outcome pathways and associated new approach methodologies.Frontiers in toxicology · 2025Article
- TheMolecular biology of the cell · 2025Article
- ATAD1 Regulates Neuronal Development and Synapse Formation Through Tuning Mitochondrial Function.International journal of molecular sciences · 2024Article
- Variability of Mitochondrial DNA Heteroplasmy: Association with Asymptomatic Carotid Atherosclerosis.Biomedicines · 2024Article
- ThebioRxiv : the preprint server for biology · 2024Article
- Ablation ofiScience · 2024Article
- Review
- Redox-Mediated Rewiring of Signalling Pathways: The Role of a Cellular Clock in Brain Health and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Manipulating mitochondrial electron flow enhances tumor immunogenicity.Science (New York, N.Y.) · 2023Article
- IF1 promotes oligomeric assemblies of sluggish ATP synthase and outlines the heterogeneity of the mitochondrial membrane potential.Communications biology · 2023Article
- The Mitochondrial ATP Synthase/IF1 Axis in Cancer Progression: Targets for Therapeutic Intervention.Cancers · 2023Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
The mitochondrial ATP synthase emerges as key hub of cellular functions controlling the production of ATP, cellular signaling, and fate. It is regulated by the ATPase inhibitory factor 1 (IF1), which is highly abundant in neurons. Herein, we ablated or overexpressed IF1 in mouse neurons to show that IF1 dose defines the fraction of active/inactive enzyme in vivo, thereby controlling mitochondrial function and the production of mitochondrial reactive oxygen species (mtROS). Transcriptomic, proteomic, and metabolomic analyses indicate that IF1 dose regulates mitochondrial metabolism, synaptic function, and cognition. Ablation of IF1 impairs memory, whereas synaptic transmission and learning are enhanced by IF1 overexpression. Mechanistically, quenching the IF1-mediated increase in mtROS production in mice overexpressing IF1 reduces the increased synaptic transmission and obliterates the learning advantage afforded by the higher IF1 content. Overall, IF1 plays a key role in neuronal function by regulating the fraction of ATP synthase responsible for mitohormetic mtROS signaling.
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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.