ArticleOncotarget2016
Rapamycin enhances survival in a Drosophila model of mitochondrial disease.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 55 citations in OpenAlex.
- Diet-dependent, beneficial and adverse effects of rapamycin on life span of Drosophila melanogaster.GeroScience · 2026Article
- Mitochondrial complex I deficiency-associated diseases and models.Cellular and molecular life sciences : CMLS · 2026Review
- Tissue-specific molecular regulation of aging mechanisms with methionine restriction in mice and the potential role of methionine sulfoxide reductase.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- Leigh Syndrome: A Comprehensive Review of the Disease and Present and Future Treatments.Biomedicines · 2025Review
- Disease models of Leigh syndrome: From yeast to organoids.Journal of inherited metabolic disease · 2024Review
- Pathways controlling neurotoxicity and proteostasis in mitochondrial complex I deficiency.Human molecular genetics · 2024Article
- Sulfur Amino Acid Restriction alters mitochondrial function depending on tissue, sex, and Methionine sulfoxide reductase A (MsrA) status.Research square · 2023Article
- Rapamycin supplementation ofRoyal Society open science · 2023Article
- Testing the evidence that lifespan-extending compound interventions are conserved across laboratory animal model species.GeroScience · 2023Review
- Rapamycin treatment early in life reprograms aging: hyperfunction theory and clinical practice.Aging · 2022Article
- Rapamycin rescues mitochondrial dysfunction in cells carrying the m.8344A > G mutation in the mitochondrial tRNAMolecular medicine (Cambridge, Mass.) · 2022Article
- Leukocytes mediate disease pathogenesis in the Ndufs4(KO) mouse model of Leigh syndrome.JCI insight · 2022Article
- Mitochondrial dynamics involves molecular and mechanical events in motility, fusion and fission.Frontiers in cell and developmental biology · 2022Review
- 5-Aminolevulinic acid and sodium ferrous citrate ameliorate muscle aging and extend healthspan in Drosophila.FEBS open bio · 2022Article
- Thermal and Oxygen Flight Sensitivity in AgeingBiology · 2021Article
- Anti-aging: senolytics or gerostatics (unconventional view).Oncotarget · 2021Review
- An energetics perspective on geroscience: mitochondrial protonmotive force and aging.GeroScience · 2021Article
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- Moving towards clinical trials for mitochondrial diseases.Journal of inherited metabolic disease · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pediatric mitochondrial disorders are a devastating category of diseases caused by deficiencies in mitochondrial function. Leigh Syndrome (LS) is the most common of these diseases with symptoms typically appearing within the first year of birth and progressing rapidly until death, usually by 6-7 years of age. Our lab has recently shown that genetic inhibition of the mechanistic target of rapamycin (TOR) rescues the short lifespan of yeast mutants with defective mitochondrial function, and that pharmacological inhibition of TOR by administration of rapamycin significantly rescues the shortened lifespan, neurological symptoms, and neurodegeneration in a mouse model of LS. However, the mechanism by which TOR inhibition exerts these effects, and the extent to which these effects can extend to other models of mitochondrial deficiency, are unknown. Here, we probe the effects of TOR inhibition in a Drosophila model of complex I deficiency. Treatment with rapamycin robustly suppresses the lifespan defect in this model of LS, without affecting behavioral phenotypes. Interestingly, this increased lifespan in response to TOR inhibition occurs in an autophagy-independent manner. Further, we identify a fat storage defect in the ND2 mutant flies that is rescued by rapamycin, supporting a model that rapamycin exerts its effects on mitochondrial disease in these animals by altering metabolism.
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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.