ArticleMolecular medicine (Cambridge, Mass.)2024
Melatonin ameliorates age-related sarcopenia by inhibiting fibrogenic conversion of satellite cell.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Modulation of satellite cell function to alleviate age-related sarcopenia: Electrical stimulation & Ca²⁺ signaling combined approach.iScience · 2026Review
- Molecular interaction mechanisms of muscle fiber type transition in aging sarcopenia and the role of exercise intervention.The Egyptian journal of internal medicine · 2026Article
- Radiation-induced impairment of skeletal muscle regeneration.Radiology and oncology · 2025Review
- Regulatory Landscapes of Muscle Satellite Cells: From Mechanism to Application.International journal of stem cells · 2025Review
- Melatonin Interplay in Physiology and Disease-The Fountain of Eternal Youth Revisited.Biomolecules · 2025Review
- Melatonin and Exercise Restore Myogenesis and Mitochondrial Dynamics Deficits Associated With Sarcopenia in iMS-Bmal1Journal of pineal research · 2025Article
- The impact of cellular senescence on aging skeletal muscle.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
The fibrogenic conversion of satellite cells contributes to the atrophy and fibrosis of skeletal muscle, playing a significant role in the pathogenesis of age-related sarcopenia. Melatonin, a hormone secreted by the pineal gland, exhibits anti-aging and anti-fibrotic effects in various conditions. However, the effect of melatonin on satellite cell fate and age-related sarcopenia remains under-explored. Here, we report that melatonin treatment mitigated the loss of muscle mass and strength in aged mice, replenished the satellite cell pool and curtailed muscle fibrosis. When primary SCs were cultured in vitro and subjected to aging induction via D-galactose, they exhibited a diminished myogenic potential and a conversion from myogenic to fibrogenic lineage. Notably, melatonin treatment effectively restored the myogenic potential and inhibited this lineage conversion. Furthermore, melatonin attenuated the expression of the fibrogenic cytokine, transforming growth factor-β1, and reduced the phosphorylation of its downstream targets Smad2/3 both in vivo and in vitro. In summary, our findings show melatonin's capacity to counteract muscle decline and inhibit fibrogenic conversion in aging SCs and highlight its potential therapeutic value for age-related sarcopenia.
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