An in vitro model to study molecular pathogenesis of sarcopenia established by a SASP-dependent human myotube culture
Ishii KA., Hashimoto R., Umeda C., Hosoyama T., Watanabe K.
Laboratory Study, published in PLoS One (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- PLoS One (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 40623060
- PMCID
- PMC12233260
- DOI
- 10.1371/journal.pone.0326968
Abstract (original English)
Sarcopenia is a condition that affects one's activities of daily livingand is rapidly increasing with the ages of the global population. However, the basic molecular mechanisms for prevention and treatment are not fully understood. Although rodent model animals have many valuable aspects for studying sarcopenia, some aspects and mechanisms differ from humans, such as immune response, metabolism, stress response, and myofiber composition. This study established a human cell-based in vitro model to elucidate the molecular mechanism by which SASP from senescence-induced human mesenchymal stem cells led to the narrowing of human myotube diameter, suggesting that this model is useful for studying sarcopenia. Gene expression profiling was performed the molecular mechanisms and devel on the model by RNA sequencing to identify genes whose expression was affected by SASP. Among these, the exposure to SASP upregulated PDK4 expression, and a PDK4 inhibitor, DCA, could increase myotube diameter and reverse SASP-mediated narrowing of the diameter. Pathway analyses suggested that SASP affected energy metabolism by activating OXPHOS and promoting the expression of mitochondrial function-related genes and mitochondrial biosynthesis factors. These results provide insights that contribute to developing new treatments for sarcopenia.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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