ArticleCirculation research2021
MTORC1-Regulated Metabolism Controlled by TSC2 Limits Cardiac Reperfusion Injury.
Article in Circulation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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
34 citing papers in PubMed, 47 citations in OpenAlex.
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- SGLT2 Inhibitors Promote Diabetic Wound Healing Via AMPK/AKT/mTORC1-Regulated Endothelial Angiogenesis.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Integrative Metabolomic and Echocardiographic Profiling Reveals Metabolic-Cardiac Structural Coupling in Yili Horses During Incremental Exercise.Animals : an open access journal from MDPI · 2026Article
- Periodontitis and cardiovascular diseases: bridging the gap through mitochondrial dysfunction.Frontiers in oral health · 2026Review
- Aerobic exercise reduces lactate accumulation and improves cardiac function after myocardial infarction.Frontiers in medicine · 2026Article
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Nucleophosmin 1 lactylation in graft kidney induces ferroptotic trigger waves that exacerbate delayed graft function.Nature communications · 2025Article
- Macrophages lacking TSC2 have mTORC1-dependent increased GPNMB and ameliorate ventricular dysfunction/remodeling after ischemia-reperfusion.Scientific reports · 2025Article
- Inhibiting CD36 palmitoylation improves cardiac function post-infarction by regulating lipid metabolic homeostasis and autophagy.Nature communications · 2025Article
- Identification and validation of hypoxia-responsive signature pathways in human cardiomyocytes.3 Biotech · 2025Article
- Unraveling the metabolic‒epigenetic nexus: a new frontier in cardiovascular disease treatment.Cell death & disease · 2025Review
- Thioflavin T in-gel staining forFrontiers in molecular biosciences · 2025Article
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- The metabolic sensor AMPK: Twelve enzymes in one.Molecular metabolism · 2024Review
- The beneficial health effects of puerarin in the treatment of cardiovascular diseases: from mechanisms to therapeutics.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- The ability of microRNAs to regulate the immune response in ischemia/reperfusion inflammatory pathways.Genes and immunity · 2024Review
- Crosstalk among Reactive Oxygen Species, Autophagy and Metabolism in Myocardial Ischemia and Reperfusion Stages.Aging and disease · 2024Review
- HSPA12A maintains aerobic glycolytic homeostasis and Histone3 lactylation in cardiomyocytes to attenuate myocardial ischemia/reperfusion injury.JCI insight · 2024Article
- mTORC1 regulates the metabolic switch of postnatal cardiomyocytes during regeneration.Journal of molecular and cellular cardiology · 2024Article
- Screening and Validation of Key Genes of Autophagy in Acute Myocardial Infarction Based on Bioinformatics.Evolutionary bioinformatics online · 2024Article
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
rationaleThe mTORC1 (mechanistic target of rapamycin complex-1) controls metabolism and protein homeostasis and is activated following ischemia reperfusion (IR) injury and by ischemic preconditioning (IPC). However, studies vary as to whether this activation is beneficial or detrimental, and its influence on metabolism after IR is little reported. A limitation of prior investigations is their use of broad gain/loss of mTORC1 function, mostly applied before ischemic stress. This can be circumvented by regulating one serine (S1365) on TSC2 (tuberous sclerosis complex) to achieve bidirectional mTORC1 modulation but only with TCS2-regulated costimulation.
objectiveWe tested the hypothesis that reduced TSC2 S1365 phosphorylation protects the myocardium against IR and is required for IPC by amplifying mTORC1 activity to favor glycolytic metabolism. METHODS AND
resultsMice with either S1365A (TSC2
conclusionsTSC2-S1365 phosphorylation status regulates myocardial substrate utilization, and its decline activates mTORC1 biasing metabolism away from fatty acid oxidation to glycolysis to confer protection against IR. This pathway is also engaged and reduced TSC2 S1365 phosphorylation required for effective IPC. Graphic Abstract: A graphic abstract is available for this article.
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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.