ArticleAging cell2015
Long-lived Snell dwarf mice display increased proteostatic mechanisms that are not dependent on decreased mTORC1 activity.
Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Influence of Nrf2 activators on subcellular skeletal muscle protein and DNA synthesis rates after 6 weeks of milk protein feeding in older adults.GeroScience · 2017Trial
- Proteomic changes induced by longevity-promoting interventions in mice.GeroScience · 2024Article
- FGF21 Induces Skeletal Muscle Atrophy and Increases Amino Acids in Female Mice: A Potential Role for Glucocorticoids.Endocrinology · 2024Article
- Short-term repeated human biopsy sampling contributes to changes in muscle morphology and higher outcome variability.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Phytochemical compound PB125 attenuates skeletal muscle mitochondrial dysfunction and impaired proteostasis in a model of musculoskeletal decline.The Journal of physiology · 2023Article
- Skeletal Muscle Nuclei in Mice are not Post-mitotic.Function (Oxford, England) · 2023Article
- Rates of protein synthesis are maintained in brain but reduced in skeletal muscle during dietary sulfur amino acid restriction.Frontiers in aging · 2022Article
- Integrated or Independent Actions of Metformin in Target Tissues Underlying Its Current Use and New Possible Applications in the Endocrine and Metabolic Disorder Area.International journal of molecular sciences · 2021Review
- Tumor burden negatively impacts protein turnover as a proteostatic process in noncancerous liver, heart, and muscle, but not brain.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Sex differences in changes of protein synthesis with rapamycin treatment are minimized when metformin is added to rapamycin.GeroScience · 2021Article
- Long-lived mice with reduced growth hormone signaling have a constitutive upregulation of hepatic chaperone-mediated autophagy.Autophagy · 2021Article
- Mouse models of growth hormone deficiency.Reviews in endocrine & metabolic disorders · 2021Review
- The mechanisms of skeletal muscle atrophy in response to transient knockdown of the vitamin D receptor in vivo.The Journal of physiology · 2021Article
- Muscle from aged rats is resistant to mechanotherapy during atrophy and reloading.GeroScience · 2021Article
- Cancer cachexia in a mouse model of oxidative stress.Journal of cachexia, sarcopenia and muscle · 2020Article
- Massage as a mechanotherapy promotes skeletal muscle protein and ribosomal turnover but does not mitigate muscle atrophy during disuse in adult rats.Acta physiologica (Oxford, England) · 2020Article
- Short-term Calorie Restriction and 17α-Estradiol Administration Elicit Divergent Effects on Proteostatic Processes and Protein Content in Metabolically Active Tissues.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
- Molecular changes associated with spinal cord aging.GeroScience · 2020Article
- Brain Protein Synthesis Rates in the UM-HET3 Mouse Following Treatment With Rapamycin or Rapamycin With Metformin.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
- Differential Effects of Rapamycin and Metformin in Combination With Rapamycin on Mechanisms of Proteostasis in Cultured Skeletal Myotubes.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Maintaining proteostasis is thought to be a key factor in slowed aging. In several growth-restricted models of long-life, we have shown evidence of increased proteostatic mechanisms, suggesting that proteostasis may be a shared characteristic of slowed aging. The Snell dwarf mouse is generated through the mutation of the Pit-1 locus causing reductions in multiple hormonal growth factors and mTORC1 signaling. Snell dwarfs are one of the longest lived rodent models of slowed aging. We hypothesized that proteostatic mechanisms would be increased in Snell compared to control (Con) as in other models of slowed aging. Using D2O, we simultaneously assessed protein synthesis in multiple subcellular fractions along with DNA synthesis in skeletal muscle, heart, and liver over 2 weeks in both sexes. We also assessed mTORC1-substrate phosphorylation. Skeletal muscle protein synthesis was decreased in all protein fractions of Snell compared to Con, varied by fraction in heart, and was not different between groups in liver. DNA synthesis was lower in Snell skeletal muscle and heart but not in liver when compared to Con. The new protein to new DNA synthesis ratio was increased threefold in Snell skeletal muscle and heart compared to Con. Snell mTORC1-substrate phosphorylation was decreased only in heart and liver. No effect of sex was seen in this study. Together with our previous investigations in long-lived models, we provide evidence further supporting proteostasis as a shared characteristic of slowed aging and show that increased proteostatic mechanisms may not necessarily require a decrease in mTORC1.
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