ArticleJournal of the American Heart Association2019
Mechanistic Target of Rapamycin Complex 1 Signaling Modulates Vascular Endothelial Function Through Reactive Oxygen Species.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 34 citations in OpenAlex.
- Vascular conditioning prevents adverse left ventricular remodelling after acute myocardial infarction: a randomised remote conditioning study.Basic research in cardiology · 2021Trial
- Endothelial Dysfunction and Metabolic Reprogramming in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2026Review
- KIF11 variants in familial exudative vitreoretinopathy leading to mTORC1 overactivation and impaired cell cycle progression.Human genomics · 2025Article
- Skeletal muscle-derived musclin attenuates glycolysis, oxidative stress, and pulmonary hypertension through the NPR3/AKT/mTORC1 pathway.Acta biochimica et biophysica Sinica · 2024Article
- Duality of Branched-Chain Amino Acids in Chronic Cardiovascular Disease: Potential Biomarkers versus Active Pathophysiological Promoters.Nutrients · 2024Review
- Beneficial effects of rapamycin on endothelial function in systemic lupus erythematosus.Frontiers in physiology · 2024Article
- The Neuroprotective Effects and Probable Mechanisms of Everolimus in a Rat Model of Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2023Article
- Proteostasis and resilience in the mechanically-stressed vascular endothelium.Current opinion in physiology · 2023Review
- KRIT1: A Traffic Warden at the Busy Crossroads Between Redox Signaling and the Pathogenesis of Cerebral Cavernous Malformation Disease.Antioxidants & redox signaling · 2023Review
- Branched-chain amino acids in cardiovascular disease.Nature reviews. Cardiology · 2023Review
- mTOR contributes to endothelium-dependent vasorelaxation by promoting eNOS expression and preventing eNOS uncoupling.Communications biology · 2022Article
- Rapamycin Suppresses Penile NADPH Oxidase Activity to Preserve Erectile Function in Mice Fed a Western Diet.Biomedicines · 2021Article
- Vascular effects of disrupting endothelial mTORC1 signaling in obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Genome-wide CRISPRi/a screens in human neurons link lysosomal failure to ferroptosis.Nature neuroscience · 2021Article
- NLRP3 Inflammasome at the Interface of Inflammation, Endothelial Dysfunction, and Type 2 Diabetes.Cells · 2021Review
- mTORC1 (Mechanistic Target of Rapamycin Complex 1) Signaling in Endothelial and Smooth Muscle Cells Is Required for Vascular Function.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Longevity genes, cardiac ageing, and the pathogenesis of cardiomyopathy: implications for understanding the effects of current and future treatments for heart failure.European heart journal · 2020Article
- Article
- Potential molecular mechanism of ACE gene at different time points in STEMI patients based on genome-wide microarray dataset.Lipids in health and disease · 2019Article
- Smooth Muscle Cell-Specific Disruption of the BBSome Causes Vascular Dysfunction.Hypertension (Dallas, Tex. : 1979) · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Background The mechanistic target of rapamycin complex 1 ( mTORC 1) is an important intracellular energy sensor that regulates gene expression and protein synthesis through its downstream signaling components, the S6-kinase and the ribosomal S6 protein. Recently, signaling arising from mTORC 1 has been implicated in regulation of the cardiovascular system with implications for disease. Here, we examined the contribution of mTORC 1 signaling to the regulation of vascular function. Methods and Results Activation of mTORC 1 pathway in aortic rings with leucine or an adenoviral vector expressing a constitutively active S6-kinase reduces endothelial-dependent vasorelaxation in an mTORC 1-dependent manner without affecting smooth muscle relaxation responses. Moreover, activation of mTORC 1 signaling in endothelial cells increases reactive oxygen species ( ROS ) generation and ROS gene expression resulting in a pro-oxidant gene environment. Blockade of ROS signaling with Tempol restores endothelial function in vascular rings with increased mTORC 1 activity indicating a crucial interaction between mTORC 1 and ROS signaling. We then tested the role of nuclear factor-κB transcriptional complex in connecting mTORC 1 and ROS signaling in endothelial cells. Blockade of inhibitor of nuclear factor κ-B kinase subunit β activity with BMS -345541 prevented the increased ROS generation associated with increased mTORC 1 activity in endothelial cells but did not improve vascular endothelial function in aortic rings with increased mTORC 1 and ROS signaling. Conclusions These results implicate mTORC 1 as a critical molecular signaling hub in the vascular endothelium in mediating vascular endothelial function through modulation of ROS signaling.
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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.