ArticleJCSM rapid communications2018
Castration induces satellite cell activation that contributes to skeletal muscle maintenance.
Article in JCSM rapid communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Androgen receptor imprints satellite cell stemness and preserves their reservoir for lifelong regeneration and optimal repair.Science advances · 2026Article
- Estrogen Receptor Regulates Male Satellite Cells in a Female, but Not Male, Environment.Cells · 2025Article
- Insights into muscle stem cell dynamics during postnatal development.The FEBS journal · 2022Review
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- Radiation-Induced Damage to Prepubertal Pax7+ Skeletal Muscle Stem Cells Drives Lifelong Deficits in Myofiber Size and Nuclear Number.iScience · 2020Article
- Chemoradiation impairs myofiber hypertrophic growth in a pediatric tumor model.Scientific reports · 2020Article
- Inhibition of inflammatory CCR2 signaling promotes aged muscle regeneration and strength recovery after injury.Nature communications · 2020Article
- Prostate tumor-derived GDF11 accelerates androgen deprivation therapy-induced sarcopenia.JCI insight · 2020Article
- Prepubertal skeletal muscle growth requires Pax7-expressing satellite cell-derived myonuclear contribution.Development (Cambridge, England) · 2018Article
- More variety with the Journal of Cachexia, Sarcopenia and Muscle: JCSM Clinical Reports and JCSM Rapid Communications have both gone live.Journal of cachexia, sarcopenia and muscle · 2018Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSarcopenia, the age-related loss of skeletal muscle, is a side effect of androgen deprivation therapy (ADT) for prostate cancer patients. Resident stem cells of skeletal muscle, satellite cells (SCs), are an essential source of progenitors for the growth and regeneration of skeletal muscle. Decreased androgen signaling and deficits in the number and function of SCs are features of aging. Although androgen signaling is known to regulate skeletal muscle, the cellular basis for ADT-induced exacerbation of sarcopenia is unknown. Furthermore, the consequences of androgen deprivation on SC fate in adult skeletal muscle remain largely unexplored.
methodsWe examined SC fate in an androgen-deprived environment using immunofluorescence and fluorescence-activated cell sorting (FACS) with SC-specific markers in young castrated mice. To study the effects of androgen deprivation on SC function and skeletal muscle regenerative capacity, young castrated mice were subjected to experimental regenerative paradigms. SC-derived-cell contributions to skeletal muscle maintenance were examined in castrated
resultsCastration led to SC activation, however this did not result in a decline in SC function or skeletal muscle regenerative capacity. Surprisingly, castration induced SC-dependent maintenance of young skeletal muscle. The functional dependence of skeletal muscles on SCs in young castrated mice was demonstrated by an increase in SC-derived-cell fusion within skeletal muscle fibers. SC depletion was associated with further atrophy and functional decline, as well as the induction of partial innervation and the loss of NMJ-associated myonuclei in skeletal muscles from castrated mice.
conclusionThe maintenance of skeletal muscles in young castrated mice relies on the cellular contributions of SCs. Considering the well-described age-related decline in SCs, the results in this study highlight the need to devise strategies that promote SC maintenance and activity to attenuate or reverse the progression of sarcopenia in elderly androgen-deprived individuals.
Indexed as
Identifiers
29782610PMC5959044W2785672002What 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.