ArticleNature communications2019
Role of p110a subunit of PI3-kinase in skeletal muscle mitochondrial homeostasis and metabolism.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Astrocytic PI3Kα controls synaptic plasticity and cognitive function via serine metabolism.Nature communications · 2026Article
- miRNAs as cell-intrinsic epigenetic regulators in muscle in type 2 diabetes.Signal transduction and targeted therapy · 2026Article
- Whole genome copy number variation analysis to detect genomic regions for resistance to Haemonchus contortus in Sheep.BMC genomics · 2026Article
- Exercise alleviates cognitive dysfunction in Alzheimer's disease mice via skeletal muscle-derived extracellular vesicles that enhance plaque clearance by microglia.Nature aging · 2026Article
- Article
- Hemifacial myohyperplasia is due to somatic muscular PIK3CA gain-of-function mutations and responds to pharmacological inhibition.The Journal of experimental medicine · 2023Article
- Maternal and Fetal PI3K-p110α Deficiency Induces Sex-Specific Changes in Conceptus Growth and Placental Mitochondrial Bioenergetic Reserve in Mice.Veterinary sciences · 2022Article
- Aerobic Exercise Prevents Chronic Inflammation and Insulin Resistance in Skeletal Muscle of High-Fat Diet Mice.Nutrients · 2022Article
- Visceral adiposity, inflammation, and hippocampal function in obesity.Neuropharmacology · 2022Review
- Ablation of PI3K-p110alpha Impairs Maternal Metabolic Adaptations to Pregnancy.Frontiers in cell and developmental biology · 2022Article
- PI3K and AKT at the Interface of Signaling and Metabolism.Current topics in microbiology and immunology · 2022Article
- Insulin and IGF-1 receptors regulate complex I-dependent mitochondrial bioenergetics and supercomplexes via FoxOs in muscle.The Journal of clinical investigation · 2021Article
- Efficacy of Providing the PI3K p110α Inhibitor BYL719 (Alpelisib) to Middle-Aged Mice in Their Diet.Biomolecules · 2021Article
- Vav2 catalysis-dependent pathways contribute to skeletal muscle growth and metabolic homeostasis.Nature communications · 2020Article
- Hyperinsulinaemia in cancer.Nature reviews. Cancer · 2020Review
- Prolonged treatment with a PI3K p110α inhibitor causes sex- and tissue-dependent changes in antioxidant content, but does not affect mitochondrial function.Bioscience reports · 2020Article
- Emerging molecular mediators and targets for age-related skeletal muscle atrophy.Translational research : the journal of laboratory and clinical medicine · 2020Review
- Review
- CORP: Using transgenic mice to study skeletal muscle physiology.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Skeletal muscle insulin resistance, decreased phosphatidylinositol 3-kinase (PI3K) activation and altered mitochondrial function are hallmarks of type 2 diabetes. To determine the relationship between these abnormalities, we created mice with muscle-specific knockout of the p110α or p110β catalytic subunits of PI3K. We find that mice with muscle-specific knockout of p110α, but not p110β, display impaired insulin signaling and reduced muscle size due to enhanced proteasomal and autophagic activity. Despite insulin resistance and muscle atrophy, M-p110αKO mice show decreased serum myostatin, increased mitochondrial mass, increased mitochondrial fusion, and increased PGC1α expression, especially PCG1α2 and PCG1α3. This leads to enhanced mitochondrial oxidative capacity, increased muscle NADH content, and higher muscle free radical release measured in vivo using pMitoTimer reporter. Thus, p110α is the dominant catalytic isoform of PI3K in muscle in control of insulin sensitivity and muscle mass, and has a unique role in mitochondrial homeostasis in skeletal muscle.
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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.