ArticleAging2013
Rapamycin doses sufficient to extend lifespan do not compromise muscle mitochondrial content or endurance.
Article in Aging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed.
- Bench to bedside: is rapamycin headed for the docTOR?GeroScience · 2026Review
- Rapamycin Does Not Compromise Exercise-Induced Muscular Adaptations in Female Mice.Aging cell · 2025Article
- Review
- Geroprotector drugs and exercise: friends or foes on healthy longevity?BMC biology · 2023Review
- Rapamycin treatment early in life reprograms aging: hyperfunction theory and clinical practice.Aging · 2022Article
- Therapeutic Antiaging Strategies.Biomedicines · 2022Review
- Anti-aging: senolytics or gerostatics (unconventional view).Oncotarget · 2021Review
- Article
- Article
- Rapamycin for longevity: opinion article.Aging · 2019Article
- Disease or not, aging is easily treatable.Aging · 2018Article
- Cardioprotective effects of dietary rapamycin on adult female C57BLKS/J-LeprAnnals of the New York Academy of Sciences · 2018Article
- Rapamycin, proliferation and geroconversion to senescence.Cell cycle (Georgetown, Tex.) · 2018Article
- Low-dose rapamycin extends lifespan in a mouse model of mtDNA depletion syndrome.Human molecular genetics · 2017Article
- From rapalogs to anti-aging formula.Oncotarget · 2017Review
- Gerosuppression by pan-mTOR inhibitors.Aging · 2016Article
- Energetic interventions for healthspan and resiliency with aging.Experimental gerontology · 2016Review
- Rapamycin Versus Intermittent Feeding: Dissociable Effects on Physiological and Behavioral Outcomes When Initiated Early and Late in Life.The journals of gerontology. Series A, Biological sciences and medical sciences · 2016Article
- Article
- Molecular mechanisms for mitochondrial adaptation to exercise training in skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
Rapamycin extends lifespan in mice, but can have a number of undesirable effects that may ultimately limit its utility in humans. The canonical target of rapamycin, and the one thought to account for its effects on lifespan, is the mammalian/mechanistic target of rapamycin, complex 1 (mTORC1). We have previously shown that at least some of the detrimental side effects of rapamycin are due to "off target" disruption of mTORC2, suggesting they could be avoided by more specific targeting of mTORC1. However, mTORC1 inhibitionper se can reduce the mRNA expression of mitochondrial genes and compromise the function of mitochondria in cultured muscle cells, implying that defects in bioenergetics might be an unavoidable consequence of targeting mTORC1 in vivo. Therefore, we tested whether rapamycin, at the same doses used to extend lifespan, affects mitochondrial function in skeletal muscle. While mitochondrial transcripts were decreased, particularly in the highly oxidative soleus muscle, we found no consistent change in mitochondrial DNA or protein levels. In agreement with the lack of change in mitochondrial components, rapamycin-treated mice had endurance equivalent to that of untreated controls, and isolated, permeabilized muscle fibers displayed similar rates of oxygen consumption. We conclude that the doses of rapamycin required to extend life do not cause overt mitochondrial dysfunction in skeletal muscle.
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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.