International journal of molecular sciences · 2026
Integrated Transcriptomic Analysis Identifies a Candidate INHBA/Activin A-Associated Macrophage-MuSC Communication Axis in Human Skeletal Muscle Ageing.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Liu Xuanchen, Li Zehui, Yuan Yutong, Si Nuo, Yin Ningbei
Аннотация
Skeletal muscle ageing is accompanied by impaired regeneration and remodelling of the multicellular niche, yet how age-related immune changes relate to altered muscle stem cell (MuSC) states in humans remains unclear. Here, we integrated bulk RNA-sequencing, scRNA-seq and an independent older adult cohort analysis to characterize age-associated changes in human skeletal muscle and identify candidate macrophage-MuSC signalling interactions. Bulk transcriptomic analysis revealed inflammatory activation, reduced mitochondrial and metabolic programmes, and increased macrophage-associated signatures in aged muscle. Single-cell analysis resolved distinct myeloid and MuSC states. Among aged myeloid populations, inflammatory macrophages exhibited the highest SenMayo score, whereas donor-level pseudobulk analysis identified age-related early-primed MuSCs (epMuSC) remodelling involving inflammatory, interferon-related, and extracellular matrix-associated programmes. Ligand-target modelling prioritized inhibin subunit beta A (INHBA)/Activin A as a candidate signal linking inflammatory macrophages to the aged epMuSC programme. This prediction was further supported by an independent older adult human muscle scRNA-seq cohort showing concordant INHBA expression in inflammatory macrophages and Activin receptor expression in epMuSCs. In primary human MuSCs, Activin A induced Activin-responsive genes and suppressed myogenic regulators, and these effects were attenuated by SB431542, a small-molecule inhibitor of ALK4/5/7 signalling. Together, these findings support a candidate INHBA-associated, cell state-resolved communication framework between inflammatory macrophages and epMuSC remodelling in aged human muscle, providing a potential link between immune remodelling and altered regenerative cell states.