Senescent myoblasts exhibit an altered exometabolome that is linked to senescence-associated secretory phenotype (SASP) signalling.
Abstract
Cellular senescence has been implicated in the aging-related dysfunction of satellite cells, the resident muscle stem cell population primarily responsible for the repair of muscle fibres. Despite being in a state of permanent cell cycle arrest, these cells remain metabolically active and release an abundance of factors that can have detrimental effects on the cellular microenvironment. This phenomenon is known as the senescence-associated secretory phenotype (SASP), and its metabolic profile is poorly characterized in senescent muscle. In the present investigation, we examined the intracellular and extracellular metabolome of C
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Research summary
The paper investigates the metabolic changes in senescent myoblasts and their connection to the senescence-associated secretory phenotype (SASP), which is relevant to understanding cellular senescence and its implications for aging and muscle repair. However, while it contributes to the characterization of senescent cells, the findings appear to be more incremental rather than groundbreaking, limiting its overall impact on the field of longevity research.
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