ArticleThe Journal of clinical investigation2022
Upregulation of mitochondrial ATPase inhibitory factor 1 (ATPIF1) mediates increased glycolysis in mouse hearts.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 46 citations in OpenAlex.
- ATPIF1, the rheostat in mitochondrial bioenergetics and dysfunction in diseases.Mitochondrion · 2026Review
- Malonic acid promotes glycolytic activity in cumulus cells and improves the quality of bovine oocytes matured in vitro.The Journal of reproduction and development · 2026Article
- ATP Synthase Inhibitory Factor-1 Deficiency Attenuates Doxorubicin Cardiotoxicity by Preserving Mitochondrial Structure and Function.International journal of molecular sciences · 2026Article
- Investigating the relationship between ATP synthase and the TCA cycle by crosslinking mass spectrometry.Nature communications · 2026Article
- Mitochondria: The Crossroads of Complement Activation and Kidney Injury Progression.International journal of molecular sciences · 2026Review
- Novel interactions between the C5-C5aR1 Axis and IF1: Implications for kidney mitochondrial physiology and ischemia-reperfusion injury.Physiological reports · 2026Article
- ATPIF1 Deficiency Significantly AlleviatesJournal of microbiology and biotechnology · 2026Article
- YY1/Asprosin/PFKP axis regulates glycolytic metabolic and exacerbates pathological cardiac hypertrophy.Nature communications · 2026Article
- Proline-Mediated Inhibition of ATPIF1-mTOR Signaling Alleviates Radiation-Induced Macrophage Polarization and Colon Inflammation.Inflammation · 2026Article
- Hyaluronic Acid-Palmitate Nanoparticle Delivery of Carbonic Anhydrase Inhibitors Impairs Growth and Early Metabolism inInternational journal of molecular sciences · 2026Article
- METTL1-Mediated NMedComm · 2026Article
- Metabolic reprogramming in cardiac fibrosis: mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 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
- Bioenergetics of cancer cells: insights into the Warburg effect and regulation of ATP synthase.Molecular medicine (Cambridge, Mass.) · 2025Article
- Automated integration of multi-slice spatial transcriptomics data in 2D and 3D using VR-Omics.Genome biology · 2025Article
- Leucine-Rich Repeat-Containing G Protein-Coupled Receptor 6 Ameliorates Pressure Overload-Induced Cardiac Hypertrophy by Regulating Cardiomyocyte Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Megakaryocytes transfer mitochondria to bone marrow mesenchymal stromal cells to lower platelet activation.The Journal of clinical investigation · 2025Article
- Large-Scale Quantitative Cross-Linking and Mass Spectrometry Provide New Insight into Protein Conformational Plasticity within Organelles, Cells, and Tissues.Journal of proteome research · 2025Article
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
In hypertrophied and failing hearts, fuel metabolism is reprogrammed to increase glucose metabolism, especially glycolysis. This metabolic shift favors biosynthetic function at the expense of ATP production. Mechanisms responsible for the switch are poorly understood. We found that inhibitory factor 1 of the mitochondrial FoF1-ATP synthase (ATPIF1), a protein known to inhibit ATP hydrolysis by the reverse function of ATP synthase during ischemia, was significantly upregulated in pathological cardiac hypertrophy induced by pressure overload, myocardial infarction, or α-adrenergic stimulation. Chemical cross-linking mass spectrometry analysis of hearts hypertrophied by pressure overload suggested that increased expression of ATPIF1 promoted the formation of FoF1-ATP synthase nonproductive tetramer. Using ATPIF1 gain- and loss-of-function cell models, we demonstrated that stalled electron flow due to impaired ATP synthase activity triggered mitochondrial ROS generation, which stabilized HIF1α, leading to transcriptional activation of glycolysis. Cardiac-specific deletion of ATPIF1 in mice prevented the metabolic switch and protected against the pathological remodeling during chronic stress. These results uncover a function of ATPIF1 in nonischemic hearts, which gives FoF1-ATP synthase a critical role in metabolic rewiring during the pathological remodeling of the heart.
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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.