ArticleJournal of molecular and cellular cardiology2019
Cardiac-specific deletion of GCN5L1 restricts recovery from ischemia-reperfusion injury.
Article in Journal of molecular and cellular cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 62 citations in OpenAlex.
- GCN5L1-Mediated Lysine Acetylation Regulates Mitochondrial Bioenergetics and Redox Homeostasis in the Aged Heart.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- GCN5L1 Inhibits Pyruvate Dehydrogenase Phosphorylation During Cardiac Ischemia-Reperfusion Injury.FASEB bioAdvances · 2025Article
- Drp1 acetylation mediated by CDK5-AMPK-GCN5L1 axis promotes cerebral ischemic injury via facilitating mitochondrial fission.Molecular medicine (Cambridge, Mass.) · 2024Article
- Mitochondrial CypD Acetylation Promotes Endothelial Dysfunction and Hypertension.Circulation research · 2024Article
- GCN5L1-mediated acetylation prevents Rictor degradation in cardiac cells after hypoxic stress.Cellular signalling · 2024Article
- 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
- Cytochrome c lysine acetylation regulates cellular respiration and cell death in ischemic skeletal muscle.Nature communications · 2023Article
- Article
- GPER-dependent estrogen signaling increases cardiac GCN5L1 expression.American journal of physiology. Heart and circulatory physiology · 2022Article
- Perfluorooctanoic acidZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Diet-induced obese mice are resistant to improvements in cardiac function resulting from short-term adropin treatment.Current research in physiology · 2022Article
- Loss of the mitochondrial phosphate carrier SLC25A3 induces remodeling of the cardiac mitochondrial protein acylome.American journal of physiology. Cell physiology · 2021Article
- The emerging roles of GCN5L1 in mitochondrial and vacuolar organelle biology.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- Increased fatty acid oxidation enzyme activity in the hearts of mice fed a high fat diet does not correlate with improved cardiac contractile function.Current research in physiology · 2020Article
- Rethinking Protein Acetylation in Pressure Overload-Induced Heart Failure.Circulation research · 2020Article
- Loss of GCN5L1 in cardiac cells disrupts glucose metabolism and promotes cell death via reduced Akt/mTORC2 signaling.The Biochemical journal · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
GCN5L1 regulates mitochondrial protein acetylation, cellular bioenergetics, reactive oxygen species (ROS) generation, and organelle positioning in a number of diverse cell types. However, the functional role of GCN5L1 in the heart is currently unknown. As many of the factors regulated by GCN5L1 play a major role in ischemia-reperfusion (I/R) injury, we sought to determine if GCN5L1 is an important nexus in the response to cardiac ischemic stress. Deletion of GCN5L1 in cardiomyocytes resulted in impaired myocardial post-ischemic function and increased infarct development in isolated work-performing hearts. GCN5L1 knockout hearts displayed hallmarks of ROS damage, and scavenging of ROS restored cardiac function and reduced infarct volume in vivo. GCN5L1 knockdown in cardiac-derived AC16 cells was associated with reduced activation of the pro-survival MAP kinase ERK1/2, which was also reversed by ROS scavenging, leading to restored cell viability. We therefore conclude that GCN5L1 activity provides an important protection against I/R induced, ROS-mediated damage in the ischemic heart.
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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.