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Oxytocin is an age-specific circulating hormone that is necessary for muscle maintenance and regeneration
Open accessAbstract
The regenerative capacity of skeletal muscle declines with age. Previous studies suggest that this process can be reversed by exposure to young circulation; however, systemic age-specific factors responsible for this phenomenon are largely unknown. Here we report that oxytocin--a hormone best known for its role in lactation, parturition and social behaviours--is required for proper muscle tissue regeneration and homeostasis, and that plasma levels of oxytocin decline with age. Inhibition of oxytocin signalling in young animals reduces muscle regeneration, whereas systemic administration of oxytocin rapidly improves muscle regeneration by enhancing aged muscle stem cell activation/proliferation through activation of the MAPK/ERK signalling pathway. We further show that the genetic lack of oxytocin does not cause a developmental defect in muscle but instead leads to premature sarcopenia. Considering that oxytocin is an FDA-approved drug, this work reveals a potential novel and safe way to combat or prevent skeletal muscle ageing.
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“As demonstrated in Figure 2, old human serum strongly reduced myogenic cell proliferation (which is consistent with the effects of the old mouse serum [1, 2, 6, 7, 13]).”
From Rejuvenation of three germ layers tissues by exchanging old blood plasma with saline-albumin (2020) · cites this paper as [13]
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“Intriguingly, at least part of the ‘rejuvenating’ effect of a young systemic environment appears related to the higher levels of circulating growth differentiation factor 11 (GDF11) and oxytocin present in young blood as compared to aged38,166,168,169.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [169]
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Metadata
- Authors
- Elabd, C., Cousin, W., Upadhyayula, P., Chen, R. Y., Chooljian, M. S., Li, J., Kung, S., Jiang, K. P., & Conboy, I. M.
- Affiliations
- QB3 (US)
- Corresponding author
- Cousin, Wendy
- Conboy, Irina M.
- Venue
- Nature Communications
- Published
- 2014-06-10
- Volume
- 5
- Issue
- 1
- Pages
- 4082-4082
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4512838
- OpenAlex
- W2169617007
- Cited by
- 411
- References
- 52
- Citations by year
- 2026: 18 · 2025: 33 · 2024: 29 · 2023: 30 · 2022: 33 · 2021: 56 · 2020: 37 · 2019: 44 · 2018: 30 · 2017: 30 · 2016: 28 · 2015: 30 · 2014: 13
- FWCI
- 13.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- SENS Research Foundation
- Siebel Stem Cell Institute
- National Institutes of Health (TG2-01164)
- National Institute on Aging (AG027252, R01AG027252)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- oxytocin, skeletal muscle aging, muscle regeneration, muscle stem cells, sarcopenia, plasma hormone levels, ERK signaling, muscle homeostasis
- MeSH terms
- Aging, Animals, Homeostasis, Oxytocin, Regeneration, Stem Cells, Muscle, Skeletal, Muscle Fibers, Skeletal, Cell Culture Techniques, MAP Kinase Signaling System, Satellite Cells, Skeletal Muscle, Cell Proliferation, Mice, Sarcopenia
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