ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Cardiac mTOR protects the heart against ischemia-reperfusion injury.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- An oral-gut microbial metabolite linksGut microbes · 2026Article
- Pathogenic Role of mTOR Signaling in Cardiometabolic Disease: Implications for Heart, Liver, and Kidney Dysfunction.Physiological research · 2025Review
- Exploring the intricate link between gut microbiota dysbiosis and the aging process: implications for age-related diseases.Gut pathogens · 2025Review
- Exogenous phosphatidylserine protects against mesenteric ischemia-reperfusion with associated Akt/mTOR pathway upregulation.Scientific reports · 2025Article
- Therapeutic Approaches Targeting Ferroptosis in Cardiomyopathy.Cardiovascular drugs and therapy · 2025Review
- Clinical Insights from Proteomics in Heart Failure.Current heart failure reports · 2025Review
- The mTOR Signaling Pathway: Key Regulator and Therapeutic Target for Heart Disease.Biomedicines · 2025Review
- The metabolic sensor AMPK: Twelve enzymes in one.Molecular metabolism · 2024Review
- Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities.Frontiers in immunology · 2024Review
- The role of ferroptosis in cell-to-cell propagation of cell death initiated from focal injury in cardiomyocytes.Life sciences · 2023Article
- Regulatory effects of trimetazidine in cardiac ischemia/reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Therapeutic implication of Sonic Hedgehog as a potential modulator in ischemic injury.Pharmacological reports : PR · 2023Review
- Zooming in and out of ferroptosis in human disease.Frontiers of medicine · 2023Review
- Apelin receptor inhibition in ischemia-reperfused mouse hearts protected by endogenous n-3 polyunsaturated fatty acids.Frontiers in pharmacology · 2023Article
- TJ-M2010-5 Attenuates Severe Myocardial Ischemia/Reperfusion Injury in Heart Transplantation by Inhibiting MyD88 Homodimerization In Vivo.Journal of cardiovascular translational research · 2022Article
- Leucine Supplementation in Cancer Cachexia: Mechanisms and a Review of the Pre-Clinical Literature.Nutrients · 2022Review
- Review
- Melatonin attenuates cerebral hypoperfusion-induced hippocampal damage and memory deficits in rats by suppressing TRPM7 channels.Saudi journal of biological sciences · 2022Article
- Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Cardiac mammalian target of rapamycin (mTOR) is necessary and sufficient to prevent cardiac dysfunction in pathological hypertrophy. However, the role of cardiac mTOR in heart failure after ischemic injury remains undefined. To address this question, we used transgenic (Tg) mice with cardiac-specific overexpression of mTOR (mTOR-Tg mice) to study ischemia-reperfusion (I/R) injury in two animal models: 1) in vivo I/R injury with transient coronary artery ligation and 2) ex vivo I/R injury in Langendorff-perfused hearts with transient global ischemia. At 28 days after I/R, mortality was lower in mTOR-Tg mice than littermate control mice [wild-type (WT) mice]. Echocardiography and MRI demonstrated that global cardiac function in mTOR-Tg mice was preserved, whereas WT mice exhibited significant cardiac dysfunction. Masson's trichrome staining showed that 28 days after I/R, the area of interstitial fibrosis was smaller in mTOR-Tg mice compared with WT mice, suggesting that adverse left ventricular remodeling is inhibited in mTOR-Tg mice. In the ex vivo I/R model, mTOR-Tg hearts demonstrated improved functional recovery compared with WT hearts. Perfusion with Evans blue after ex vivo I/R yielded less staining in mTOR-Tg hearts than WT hearts, indicating that mTOR overexpression inhibited necrosis during I/R injury. Expression of proinflammatory cytokines, including IL-6 and TNF-α, in mTOR-Tg hearts was lower than in WT hearts. Consistent with this, IL-6 in the effluent post-I/R injury was lower in mTOR-Tg hearts than in WT hearts. These findings suggest that cardiac mTOR overexpression in the heart is sufficient to provide substantial cardioprotection against I/R injury and suppress the inflammatory response.
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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.