ReviewAutophagy2012
Rapamycin activates autophagy in Hutchinson-Gilford progeria syndrome: implications for normal aging and age-dependent neurodegenerative disorders.
Review in Autophagy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Who cites it
45 citing papers in PubMed, 83 citations in OpenAlex.
- HMGA1-HP1β axis regulates premature aging in Hutchinson-Gilford progeria syndrome through chromatin remodeling.Nature communications · 2026Article
- Tailored brain metastatic tumor cells-derived apoptotic bodies ameliorate Alzheimer's disease by promoting microglia efferocytosis and neuroinflammation mitigation.Journal of nanobiotechnology · 2025Article
- Impact of miR-181a on SIRT1 Expression and Senescence in Hutchinson-Gilford Progeria Syndrome.Diseases (Basel, Switzerland) · 2025Article
- Targeting CRM1 for Progeria Syndrome Therapy.Aging cell · 2025Article
- Signal-Sustained Imaging of Mitophagy with an Enzyme-Activatable Metabolic Lipid Labeling Probe.Autophagy · 2024Article
- A common molecular and cellular pathway in developing Alzheimer and cancer.Biochemistry and biophysics reports · 2024Review
- Pathogenic hyperactivation of mTORC1 by cytoplasmic EP300 in Hutchinson-Gilford progeria syndrome.Cell stress · 2024Article
- Molecular and therapeutic insights of rapamycin: a multi-faceted drug from Streptomyces hygroscopicus.Molecular biology reports · 2023Review
- Lonafarnib and everolimus reduce pathology in iPSC-derived tissue engineered blood vessel model of Hutchinson-Gilford Progeria Syndrome.Scientific reports · 2023Article
- De novo design of a novel AIE fluorescent probe tailored to autophagy visualization via pH manipulation.Biomaterials research · 2023Article
- Article
- Peripheral tissular analysis of rapamycin's effect as a neuroprotective agent in vivo.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Status of treatment strategies for Hutchinson-Gilford progeria syndrome with a focus on prelamin: A posttranslational modification.Basic & clinical pharmacology & toxicology · 2022Review
- Translational control in cell ageing: an update.Biochemical Society transactions · 2021Review
- An organelle-directed chemical ligation approach enables dual-color detection of mitophagy.Autophagy · 2021Article
- Still Living Better through Chemistry: An Update on Caloric Restriction and Caloric Restriction Mimetics as Tools to Promote Health and Lifespan.International journal of molecular sciences · 2020Review
- Peroxisomal abnormalities and catalase deficiency in Hutchinson-Gilford Progeria Syndrome.Aging · 2020Article
- Mechanistic target of rapamycin signaling in mouse models of accelerated aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Review
- Alzheimer's Disease and Cancer: When Two Monsters Cannot Be Together.Frontiers in neuroscience · 2019Article
- Farnesyltransferase inhibitor and rapamycin correct aberrant genome organisation and decrease DNA damage respectively, in Hutchinson-Gilford progeria syndrome fibroblasts.Biogerontology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
While rapamycin has been in use for years in transplant patients as an antirejection drug, more recently it has shown promise in treating diseases of aging, such as neurodegenerative disorders and atherosclerosis. We recently reported that rapamycin reverses the cellular phenotype of fibroblasts from children with the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). We found that the causative aberrant protein, progerin, was cleared through autophagic mechanisms when the cells were treated with rapamycin, suggesting a new potential treatment for HGPS. Recent evidence shows that progerin is also present in aged tissues of healthy individuals, suggesting that progerin may contribute to physiological aging. While it is intriguing to speculate that rapamycin may affect normal aging in humans, as it does in lower organisms, it will be important to identify safer analogues of rapamycin for chronic treatments in humans in order to minimize toxicity. In addition to its role in HGPS and normal aging, we discuss the potential of rapamycin for the treatment of age-dependent neurodegenerative diseases.
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What OpenQuestion holds
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.