Cellular senescence mediates facioscapulohumeral muscular dystrophy.

Cellular senescence programs in facioscapulohumeral muscular dystrophy muscle is linked to DUX4 activity and clinical severity, including in STIR-negative prodystrophic tissue.

• Why it matters: The field lacks mechanisms explaining how low, sporadic DUX4 expression progresses to muscle degeneration, and there is a need for early biomarkers before overt inflammation appears.
• What they did: Patient muscle transcriptomes were analyzed for senescence and senescence-associated secretory phenotype (SASP) enrichment, and an FSHD mouse model tested whether DUX4-induced injury triggers senescence expansion.
• The result: In mice, senescence expanded with fibroadipogenic progenitors and macrophages as major SASP sources, and lamivudine (3TC) reduced senescence, inflammation, and fibrosis while promoting regeneration.

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