ArticleNature communications2017
Vps34 PI 3-kinase inactivation enhances insulin sensitivity through reprogramming of mitochondrial metabolism.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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.
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Who cites it
49 citing papers in PubMed, 77 citations in OpenAlex.
- Nuclear class 3 PI3K co-activates fasting-specific chromatin remodelling.Nature cell biology · 2026Article
- Skeletal muscle H3K18 lactylation inhibits hepatic gluconeogenesis through IL-6 mediated interorgan communication.Science advances · 2026Article
- Pathological changes and therapeutic strategies for sarcopenia.EFORT open reviews · 2026Review
- PIKI-1, a class II PI 3-kinase, functions in endocytic trafficking.PLoS genetics · 2026Article
- Review
- Membrane receptors cluster phosphatidylserine to activate LC3-associated phagocytosis.Nature cell biology · 2025Article
- Autophagy-Targeting Nanomedicine: Strike at the Heart of the Cancer via Precise Modulation of Autophagy.Exploration (Beijing, China) · 2025Review
- LRBA deficiency impairs autophagy and contributes to enhanced antigen presentation and T-cell dysregulation.EMBO reports · 2025Article
- Autophagy repression by antigen and cytokines shapes mitochondrial, migration and effector machinery in CD8 T cells.Nature immunology · 2025Article
- Therapeutic applications of stem cell-derived exosomes in radiation-induced lung injury.Cancer cell international · 2024Review
- Regulatory Mechanisms Governing the Autophagy-Initiating VPS34 Complex and Its inhibitors.Biomolecules & therapeutics · 2024Review
- Genome-wide CRISPR/Cas9 screen identifies SLC39A9 and PIK3C3 as crucial entry factors for Ebola virus infection.PLoS pathogens · 2024Article
- Lack of phosphatidylinositol 3-kinase VPS34 in regulatory T cells leads to a fatal lymphoproliferative disorder without affecting their development.Frontiers in immunology · 2024Article
- Class 3 PI3K coactivates the circadian clock to promote rhythmic de novo purine synthesis.Nature cell biology · 2023Article
- Beyond PI3Ks: targeting phosphoinositide kinases in disease.Nature reviews. Drug discovery · 2023Review
- Targeting Class I-II-III PI3Ks in Cancer Therapy: Recent Advances in Tumor Biology and Preclinical Research.Cancers · 2023Review
- Lipid kinase PIK3C3 maintains healthy brown and white adipose tissues to prevent metabolic diseases.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- VPS34-dependent control of apical membrane function of proximal tubule cells and nutrient recovery by the kidney.Science signaling · 2022Article
- EID3 Promotes Glioma Cell Proliferation and Survival by Inactivating AMPKα1.Journal of Korean Neurosurgical Society · 2022Article
- Inhibition of Vps34 and p110δ PI3K Impairs Migration, Invasion and Three-Dimensional Spheroid Growth in Breast Cancer Cells.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
28 authors at 12 institutions in 4 countries.
Funding
Abstract
Vps34 PI3K is thought to be the main producer of phosphatidylinositol-3-monophosphate, a lipid that controls intracellular vesicular trafficking. The organismal impact of systemic inhibition of Vps34 kinase activity is not completely understood. Here we show that heterozygous Vps34 kinase-dead mice are healthy and display a robustly enhanced insulin sensitivity and glucose tolerance, phenotypes mimicked by a selective Vps34 inhibitor in wild-type mice. The underlying mechanism of insulin sensitization is multifactorial and not through the canonical insulin/Akt pathway. Vps34 inhibition alters cellular energy metabolism, activating the AMPK pathway in liver and muscle. In liver, Vps34 inactivation mildly dampens autophagy, limiting substrate availability for mitochondrial respiration and reducing gluconeogenesis. In muscle, Vps34 inactivation triggers a metabolic switch from oxidative phosphorylation towards glycolysis and enhanced glucose uptake. Our study identifies Vps34 as a new drug target for insulin resistance in Type-2 diabetes, in which the unmet therapeutic need remains substantial.
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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.