Epigenetic Rescue of Disuse Muscle Atrophy by Histone Deacetylase Inhibitor Trichostatin A

In a murine hindlimb suspension model, 14 days of unloading disrupts locomotion, muscle morphology, and nuclear architecture, but systemic Trichostatin A partially preserves them.

• Why it matters: Mechanical unloading rapidly triggers disuse muscle deterioration, yet the connection between lost mechanical input, nuclear/chromatin remodeling, and HDAC-sensitive transcriptional programs is unclear.
• What they did: Mice underwent 14 days of hindlimb suspension, then received systemic Trichostatin A; locomotor activity, super-resolution Lamin A/C and H3K9me3 heterochromatin foci, and transcriptomic/pathway shifts were quantified.
• The result: TSA significantly attenuated locomotor decline, shifted expression toward baseline, dose-dependently reversed FOXO catabolic, inflammatory, and extracellular matrix signatures, enhanced mitochondrial oxidative phosphorylation, and partially preserved nuclear lamina and H3K9me3 heterochromatin, without preventing trabecular bone loss.

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