ArticleThe Biochemical journal2019
Loss of GCN5L1 in cardiac cells disrupts glucose metabolism and promotes cell death via reduced Akt/mTORC2 signaling.
Article in The Biochemical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 64 citations in OpenAlex.
- Triphenylphosphonium compounds preferentially inhibit long-chain fatty acid oxidation in cardiac mitochondria.Research square · 2026Article
- BLOC1S1 regulates autolysosomal and exosomal dynamics during CD4bioRxiv : the preprint server for biology · 2026Article
- METTL3-m6A-SLC25A11 Axis Promotes Chronic Hypoxia-Induced Cardiomyocyte Ferroptosis.Journal of the American Heart Association · 2026Article
- GCN5L1 Aggravates Postherpetic Neuralgia Through Regulating Microglial Mitochondrial Fission-Fusion Homeostasis.Journal of cellular and molecular medicine · 2025Article
- GCN5L1 Inhibits Pyruvate Dehydrogenase Phosphorylation During Cardiac Ischemia-Reperfusion Injury.FASEB bioAdvances · 2025Article
- Zhuangyao Jianshen Wan ameliorates senile osteoporosis in SAMP6 mice through Modulation of the GCN5L1-mediated PI3K/Akt/wnt signaling pathway.Journal of orthopaedic translation · 2024Article
- GCN5L1-mediated acetylation prevents Rictor degradation in cardiac cells after hypoxic stress.Cellular signalling · 2024Article
- The mTORC2 signaling network: targets and cross-talks.The Biochemical journal · 2024Review
- GCN5L1 regulates pulmonary surfactant production by modulating lamellar body biogenesis and trafficking in mouse alveolar epithelial cells.Cellular & molecular biology letters · 2023Article
- GCN5L1-mediated acetylation prevents Rictor degradation in cardiac cells after hypoxic stress.bioRxiv : the preprint server for biology · 2023Article
- Fibroblast-to-cardiomyocyte lactate shuttle modulates hypertensive cardiac remodelling.Cell & bioscience · 2023Article
- The endo-lysosomal regulatory protein BLOC1S1 modulates hepatic lysosomal content and lysosomal lipolysis.Biochemical and biophysical research communications · 2023Article
- GCN5L1 impairs diastolic function in mice exposed to a high fat diet by restricting cardiac pyruvate oxidation.Physiological reports · 2022Article
- Article
- GPER-dependent estrogen signaling increases cardiac GCN5L1 expression.American journal of physiology. Heart and circulatory physiology · 2022Article
- Regulation and metabolic functions of mTORC1 and mTORC2.Physiological reviews · 2021Review
- Considerations for using isolated cell systems to understand cardiac metabolism and biology.Journal of molecular and cellular cardiology · 2021Review
- The emerging roles of GCN5L1 in mitochondrial and vacuolar organelle biology.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Protective effects of dexmedetomidine on hypoxia/reoxygenation injury in cardiomyocytes by regulating the CHOP signaling pathway.Molecular medicine reports · 2020Article
- Calreticulin expression in human cardiac myocytes induces ER stress-associated apoptosis.Physiological reports · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
GCN5L1 regulates protein acetylation and mitochondrial energy metabolism in diverse cell types. In the heart, loss of GCN5L1 sensitizes the myocardium to injury from exposure to nutritional excess and ischemia/reperfusion injury. This phenotype is associated with the reduced acetylation of metabolic enzymes and elevated mitochondrial reactive oxygen species (ROS) generation, although the direct molecular targets of GCN5L1 remain largely unknown. In this study, we sought to determine the mechanism by which GCN5L1 impacts energy substrate utilization and mitochondrial health. We find that hypoxia and reoxygenation (H/R) leads to a reduction in cell viability and Akt phosphorylation in GCN5L1 knockdown AC16 cardiomyocytes, in parallel with elevated glucose utilization and impaired fatty acid use. We demonstrate that glycolysis is uncoupled from glucose oxidation under normoxic conditions in GCN5L1-depleted cells. We show that GCN5L1 directly binds to the Akt-activating mTORC2 component Rictor, and that loss of Rictor acetylation is evident in GCN5L1 knockdown cells. Finally, we show that restoring Rictor acetylation in GCN5L1-depleted cells reduces mitochondrial ROS generation and increases cell survival in response to H/R. These studies suggest that GCN5L1 may play a central role in energy substrate metabolism and cell survival via the regulation of Akt/mTORC2 signaling.
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