ArticleGeroScience2018
Rapamycin increases oxidative metabolism and enhances metabolic flexibility in human cardiac fibroblasts.
Article in GeroScience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
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- Impact of MnTBAP and Baricitinib Treatment on Hutchinson-Gilford Progeria Fibroblasts.Pharmaceuticals (Basel, Switzerland) · 2022Article
- The methyltransferase enzymes KMT2D, SETD1B, and ASH1L are key mediators of both metabolic and epigenetic changes during cellular senescence.Molecular biology of the cell · 2022Article
- The role of cellular senescence in female reproductive aging and the potential for senotherapeutic interventions.Human reproduction update · 2022Review
- Mechanisms of RPE senescence and potential role of αB crystallin peptide as a senolytic agent in experimental AMD.Experimental eye research · 2022Article
- Effects of metformin, rapamycin, and resveratrol on cellular metabolism of canine primary fibroblast cells isolated from large and small breeds as they age.GeroScience · 2021Article
- Baricitinib, a JAK-STAT Inhibitor, Reduces the Cellular Toxicity of the Farnesyltransferase Inhibitor Lonafarnib in Progeria Cells.International journal of molecular sciences · 2021Article
- SQLE Mediates Metabolic Reprogramming to Promote LN Metastasis in Castration-Resistant Prostate Cancer.OncoTargets and therapy · 2021Article
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- Novel roles of immunometabolism and nonmyocyte metabolism in cardiac remodeling and injury.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Review
- COVID-19-associated cardiovascular morbidity in older adults: a position paper from the Italian Society of Cardiovascular Researches.GeroScience · 2020Review
- Inhibition of PLK4 might enhance the anti-tumour effect of bortezomib on glioblastoma via PTEN/PI3K/AKT/mTOR signalling pathway.Journal of cellular and molecular medicine · 2020Article
- Nitric oxide synthase inhibitors negatively regulate respiration in isolated rodent cardiac and brain mitochondria.American journal of physiology. Heart and circulatory physiology · 2020Article
- In vivo assessment of mitochondrial capacity using NIRS in locomotor muscles of young and elderly males with similar physical activity levels.GeroScience · 2020Article
- CC-223, NSC781406, and BGT226 Exerts a Cytotoxic Effect Against Pancreatic Cancer Cells via mTOR Signaling.Frontiers in pharmacology · 2020Article
- Amino Acid Degrading Enzymes and Autophagy in Cancer Therapy.Frontiers in pharmacology · 2020Review
- Mammalian Mitophagosome Formation: A Focus on the Early Signals and Steps.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Inhibition of mTOR signaling using rapamycin has been shown to increase lifespan and healthspan in multiple model organisms; however, the precise mechanisms for the beneficial effects of rapamycin remain uncertain. We have previously reported that rapamycin delays senescence in human cells and that enhanced mitochondrial biogenesis and protection from mitochondrial stress is one component of the benefit provided by rapamycin treatment. Here, using two models of senescence, replicative senescence and senescence induced by the presence of the Hutchinson-Gilford progeria lamin A mutation, we report that senescence is accompanied by elevated glycolysis and increased oxidative phosphorylation, which are both reduced by rapamycin. Measurements of mitochondrial function indicate that direct mitochondria targets of rapamycin are succinate dehydrogenase and matrix alanine aminotransferase. Elevated activity of these enzymes could be part of complex mechanisms that enable mitochondria to resume their optimal oxidative phosphorylation and resist senescence. This interpretation is supported by the fact that rapamycin-treated cultures do not undergo a premature senescence in response to the replacement of glucose with galactose in the culture medium, which forces a greater reliance on oxidative phosphorylation. Additionally, long-term treatment with rapamycin increases expression of the mitochondrial carrier protein UCP2, which facilitates the movement of metabolic intermediates across the mitochondrial membrane. The results suggest that rapamycin impacts mitochondrial function both through direct interaction with the mitochondria and through altered gene expression of mitochondrial carrier proteins.
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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.