ArticleAmerican journal of physiology. Cell physiology2010
mTOR attenuates the inflammatory response in cardiomyocytes and prevents cardiac dysfunction in pathological hypertrophy.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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80 citing papers in PubMed, 133 citations in OpenAlex.
- Inhibition of Egr2 Protects against TAC-induced Heart Failure in Mice by Suppressing Inflammation and Apoptosis Via Targeting Acot1 in Cardiomyocytes.Journal of cardiovascular translational research · 2025Article
- Clinical Insights from Proteomics in Heart Failure.Current heart failure reports · 2025Review
- Cellular senescence in age-related cardiovascular disease: past and future.Frontiers in aging · 2025Review
- Ubiquitin specific protease 38 aggravates pathological cardiac remodeling by stabilizing phospho-TBK1.International journal of biological sciences · 2024Article
- The role of ferroptosis in cell-to-cell propagation of cell death initiated from focal injury in cardiomyocytes.Life sciences · 2023Article
- Promising Therapeutic Treatments for Cardiac Fibrosis: Herbal Plants and Their Extracts.Cardiology and therapy · 2023Review
- MicroRNA-216a is essential for cardiac angiogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Coronary Artery Spasm-Related Heart Failure Syndrome: Literature Review.International journal of molecular sciences · 2023Review
- Leucine Supplementation in Cancer Cachexia: Mechanisms and a Review of the Pre-Clinical Literature.Nutrients · 2022Review
- Intercellular transfer of miR-200c-3p impairs the angiogenic capacity of cardiac endothelial cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Review
- Review
- Huntington's disease phenotypes are improved via mTORC1 modulation by small molecule therapy.PloS one · 2022Article
- The Potential of Hsp90 in Targeting Pathological Pathways in Cardiac Diseases.Journal of personalized medicine · 2021Review
- Inhibition of the canonical Wnt signaling pathway by a β-catenin/CBP inhibitor prevents heart failure by ameliorating cardiac hypertrophy and fibrosis.Scientific reports · 2021Article
- mTOR-mediated calcium transients affect cardiac function in ex vivo ischemia-reperfusion injury.Physiological reports · 2021Article
- SiglecF(HI) Marks Late-Stage Neutrophils of the Infarcted Heart: A Single-Cell Transcriptomic Analysis of Neutrophil Diversification.Journal of the American Heart Association · 2021Article
- Protective Role of Polyphenols in Heart Failure: Molecular Targets and Cellular Mechanisms Underlying Their Therapeutic Potential.International journal of molecular sciences · 2021Review
- TOR Signaling Pathway in Cardiac Aging and Heart Failure.Biomolecules · 2021Review
- Resistance Exercise and Whey Protein Supplementation Reduce Mechanical Allodynia and Spinal Microglia Activation After Acute Muscle Trauma in Rats.Frontiers in pharmacology · 2021Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Previous studies have suggested that inhibition of the mammalian target of rapamycin (mTOR) by rapamycin suppresses myocardial hypertrophy. However, the role of mTOR in the progression of cardiac dysfunction in pathological hypertrophy has not been fully defined. Interestingly, recent reports indicate that the inflammatory response, which plays an important role in the development of heart failure, is enhanced by rapamycin under certain conditions. Our aim in this study was to determine the influence of mTOR on pathological hypertrophy and to assess whether cardiac mTOR regulates the inflammatory response. We generated transgenic mice with cardiac-specific overexpression of wild-type mTOR (mTOR-Tg). mTOR-Tg mice were protected against cardiac dysfunction following left ventricular pressure overload induced by transverse aortic constriction (TAC) (P < 0.01) and had significantly less interstitial fibrosis compared with littermate controls (WT) at 4 wk post-TAC (P < 0.01). In contrast, TAC caused cardiac dysfunction in WT. At 1 wk post-TAC, the proinflammatory cytokines interleukin (IL)-1β and IL-6 were significantly increased in WT mice but not in mTOR-Tg mice. To further characterize the effects of mTOR activation, we exposed HL-1 cardiomyocytes transfected with mTOR to lipopolysaccharide (LPS). mTOR overexpression suppressed LPS-induced secretion of IL-6 (P < 0.001), and the mTOR inhibitors rapamycin and PP242 abolished this inhibitory effect of mTOR. In addition, mTOR overexpression reduced NF-κB-regulated transcription in HL-1 cells. These data suggest that mTOR mitigates adverse outcomes of pressure overload and that this cardioprotective effect of mTOR is mediated by regulation of the inflammatory reaction.
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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.