ArticleAging cell2019
Hypothalamic mTORC2 is essential for metabolic health and longevity.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed, 60 citations in OpenAlex.
- The role of mTORC2/RICTOR in immune cells and inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- The hallmarks of protein and amino acid restriction in aging and longevity.Cell press blue · 2026Article
- Bench to bedside: is rapamycin headed for the docTOR?GeroScience · 2026Review
- Regulation of survival, growth, and metabolism by neuronal mTOR.GeroScience · 2026Article
- Metabolic regulation by tanycyte-derived extracellular vesicles through insulin precursor-mediated neuronal recognition and mTORC component delivery.Nature metabolism · 2026Article
- Rapamycin Does Not Compromise Exercise-Induced Muscular Adaptations in Female Mice.Aging cell · 2025Article
- Establishment and application of a zebrafish model of Werner syndrome identifies sapanisertib as a potential antiaging drug.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Circadian system and aging: where both times interact.Frontiers in aging · 2025Review
- Physiological and Pathological Role of mTOR Signaling in Astrocytes.Neurochemical research · 2024Review
- Role of the central nervous system in cell non-autonomous signaling mechanisms of aging and longevity in mammals.The journal of physiological sciences : JPS · 2024Review
- The intersection of frailty and metabolism.Cell metabolism · 2024Review
- Decoding the secrets of longevity: unraveling nutraceutical and miRNA-Mediated aging pathways and therapeutic strategies.Frontiers in aging · 2024Review
- Geroprotector drugs and exercise: friends or foes on healthy longevity?BMC biology · 2023Review
- Changes of Signaling Pathways in Hypothalamic Neurons with Aging.Current issues in molecular biology · 2023Review
- Blazing a trail for the clinical use of rapamycin as a geroprotecTOR.GeroScience · 2023Article
- Regulation of metabolic health by dietary histidine in mice.The Journal of physiology · 2023Article
- Targeting the biology of aging with mTOR inhibitors.Nature aging · 2023Review
- Reduced insulin signaling in neurons induces sex-specific health benefits.Science advances · 2023Article
- mTOR Complex 1 Content and Regulation Is Adapted to Animal Longevity.International journal of molecular sciences · 2022Review
- Novel roles of mTORC2 in regulation of insulin secretion by actin filament remodeling.American journal of physiology. Endocrinology and metabolism · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 4 institutions in 1 country.
Funding
Abstract
The mechanistic target of rapamycin (mTOR) is an evolutionarily conserved protein kinase that regulates growth and metabolism. mTOR is found in two protein complexes, mTORC1 and mTORC2, that have distinct components and substrates and are both inhibited by rapamycin, a macrolide drug that robustly extends lifespan in multiple species including worms and mice. Although the beneficial effect of rapamycin on longevity is generally attributed to reduced mTORC1 signaling, disruption of mTORC2 signaling can also influence the longevity of worms, either positively or negatively depending on the temperature and food source. Here, we show that loss of hypothalamic mTORC2 signaling in mice decreases activity level, increases the set point for adiposity, and renders the animals susceptible to diet-induced obesity. Hypothalamic mTORC2 signaling normally increases with age, and mice lacking this pathway display higher fat mass and impaired glucose homeostasis throughout life, become more frail with age, and have decreased overall survival. We conclude that hypothalamic mTORC2 is essential for the normal metabolic health, fitness, and lifespan of mice. Our results have implications for the use of mTORC2-inhibiting pharmaceuticals in the treatment of brain cancer and diseases of aging.
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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.