ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Cardiac mTOR rescues the detrimental effects of diet-induced obesity in the heart after ischemia-reperfusion.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- The role of ferroptosis in cell-to-cell propagation of cell death initiated from focal injury in cardiomyocytes.Life sciences · 2023Article
- Deficiency of ataxia-telangiectasia mutated kinase attenuates Western-type diet-induced cardiac dysfunction in female mice.Physiological reports · 2022Article
- Exogenous ANP Treatment Ameliorates Myocardial Insulin Resistance and Protects against Ischemia-Reperfusion Injury in Diet-Induced Obesity.International journal of molecular sciences · 2022Article
- Extracellular vesicle-based interorgan transport of mitochondria from energetically stressed adipocytes.Cell metabolism · 2021Article
- Article
- Targeting Ferroptosis against Ischemia/Reperfusion Cardiac Injury.Antioxidants (Basel, Switzerland) · 2021Review
- Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).Journal of translational medicine · 2021Review
- mTOR-mediated calcium transients affect cardiac function in ex vivo ischemia-reperfusion injury.Physiological reports · 2021Article
- The effects of Tel2 on cardiomyocyte survival.Life sciences · 2019Article
- Cardiac ischemia-reperfusion injury under insulin-resistant conditions: SGLT1 but not SGLT2 plays a compensatory protective role in diet-induced obesity.Cardiovascular diabetology · 2019Article
- Protective Role of mTOR in Liver Ischemia/Reperfusion Injury: Involvement of Inflammation and Autophagy.Oxidative medicine and cellular longevity · 2019Review
- Protective effects of the mechanistic target of rapamycin against excess iron and ferroptosis in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2018Article
- Mammalian target of rapamycin inhibition attenuates myocardial ischaemia-reperfusion injury in hypertrophic heart.Journal of cellular and molecular medicine · 2018Article
- MiR-26a-5p regulates cardiac fibroblasts collagen expression by targeting ULK1.Scientific reports · 2018Article
- Pathological Roles of Iron in Cardiovascular Disease.Current drug targets · 2018Review
- The mTOR Signaling Pathway in Myocardial Dysfunction in Type 2 Diabetes Mellitus.Current diabetes reports · 2017Review
- Ghrelin protected neonatal rat cardiomyocyte against hypoxia/reoxygenation injury by inhibiting apoptosis through Akt-mTOR signal.Molecular biology reports · 2017Article
- Insights for Oxidative Stress and mTOR Signaling in Myocardial Ischemia/Reperfusion Injury under Diabetes.Oxidative medicine and cellular longevity · 2017Review
- Rodent Working Heart Model for the Study of Myocardial Performance and Oxygen Consumption.Journal of visualized experiments : JoVE · 2016Article
- Insulin-like growth factors and their potential role in cardiac epigenetics.Journal of cellular and molecular medicine · 2016Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Diet-induced obesity deteriorates the recovery of cardiac function after ischemia-reperfusion (I/R) injury. While mechanistic target of rapamycin (mTOR) is a key mediator of energy metabolism, the effects of cardiac mTOR in ischemic injury under metabolic syndrome remains undefined. Using cardiac-specific transgenic mice overexpressing mTOR (mTOR-Tg mice), we studied the effect of mTOR on cardiac function in both ex vivo and in vivo models of I/R injury in high-fat diet (HFD)-induced obese mice. mTOR-Tg and wild-type (WT) mice were fed a HFD (60% fat by calories) for 12 wk. Glucose intolerance and insulin resistance induced by the HFD were comparable between WT HFD-fed and mTOR-Tg HFD-fed mice. Functional recovery after I/R in the ex vivo Langendorff perfusion model was significantly lower in HFD-fed mice than normal chow diet-fed mice. mTOR-Tg mice demonstrated better cardiac function recovery and had less of the necrotic markers creatine kinase and lactate dehydrogenase in both feeding conditions. Additionally, mTOR overexpression suppressed expression of proinflammatory cytokines, including IL-6 and TNF-α, in both feeding conditions after I/R injury. In vivo I/R models showed that at 1 wk after I/R, HFD-fed mice exhibited worse cardiac function and larger myocardial scarring along myofibers compared with normal chow diet-fed mice. In both feeding conditions, mTOR overexpression preserved cardiac function and prevented myocardial scarring. These findings suggest that cardiac mTOR overexpression is sufficient to prevent the detrimental effects of diet-induced obesity on the heart after I/R, by reducing cardiac dysfunction and myocardial scarring.
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