Pharmacological researchSep 16, 2026

Aging of muscle-supporting cells through specific protein changes slows muscle healing after steroid injury

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 17, 2026

Abstract

Glucocorticoid treatment leads to cellular senescence in fibro-adipogenic progenitors (FAPs), contributing to muscle injury.

Glucocorticoids are associated with muscle atrophy and dysfunction due to their impact on FAPs.
The accumulation of senescent FAPs in skeletal muscle is linked to glucocorticoid exposure.
Increased expression of GFPT2 through STAT5A is observed following glucocorticoid treatment, enhancing O-GlcNAcylation and promoting FAP senescence.
Senescent FAPs derived from glucocorticoid treatment inhibit myotube formation, affecting skeletal muscle regrowth.
These senescent FAPs may reduce the pool of muscle stem cells by inhibiting their proliferation, potentially impairing muscle recovery.

Simplified

The clinical use of glucocorticoids often leads to skeletal muscle injury, characterized by muscle atrophy and dysfunction. Fibro-adipogenic progenitors (FAPs) play an important role in maintaining muscle homeostasis, but their roles in the recovery of skeletal muscle after glucocorticoid-induced injury remain largely elusive. Here, we reveal that glucocorticoid induces cellular senescence of FAPs, leading to their accumulation in skeletal muscle. Mechanistically, glucocorticoid enhances the expression of GFPT2 through STAT5A, which further elevates O-GlcNAcylation in FAPs and promotes their senescence. Targeting the STAT5A-GFPT2-mediated O-GlcNAcylation can reduce the burden of senescent FAPs in glucocorticoid-treated muscle and facilitate muscle recovery after injury. Our results demonstrate that exosomes derived from senescent FAPs suppress myotube formation, greatly inhibiting the regrowth of glucocorticoid-treated skeletal muscle. Moreover, senescent FAPs reduce the muscle stem cells (MuSCs) pool by suppressing their proliferation, thereby impairing the regenerative capacity of skeletal muscle during the recovery process after glucocorticoid treatment.

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Aging of muscle-supporting cells through specific protein changes slows muscle healing after steroid injury

Abstract

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