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Updated: May 16, 2026
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Evaluation of Injury-induced Senescence and In Vivo Reprogramming in the Skeletal Muscle
Published on: October 26, 2017
Brain senescence drives sarcopenia-like transcriptomic remodeling in skeletal muscle
Shoba Ekambaram1,2, Roland Patai1,2,3, Rafal Gulej1,2,3
1Vascular Cognitive Impairment and Neurodegeneration Program, Oklahoma Center for Geroscience and Healthy Brain Aging, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Geroscience
|May 14, 2026
Summary
Brain senescence can trigger aging-like changes in skeletal muscles, suggesting the brain regulates muscle aging. This discovery offers new therapeutic targets for age-related muscle decline and frailty.
Area of Science:
- Gerontology
- Neuroscience
- Muscle Physiology
Background:
- Aging causes skeletal muscle decline (sarcopenia), impacting mobility and health in older adults.
- While local factors are known, systemic processes coordinating aging across organs are increasingly recognized.
- The brain's role in regulating organismal aging is established, but its specific impact on skeletal muscle aging is unclear.
Purpose of the Study:
- To investigate if senescence (cellular aging) confined to the brain can induce aging-like changes in skeletal muscle.
- To explore the systemic mechanisms by which brain aging influences peripheral tissues.
Main Methods:
- Young mice underwent whole-brain irradiation (WBI) to induce brain senescence.
- Skeletal muscle (quadriceps) transcriptomic profiling was performed two months post-WBI.
- Gene expression data were compared to naturally aged mice.
Main Results:
- WBI induced significant gene expression changes in skeletal muscle, mimicking natural aging.
- Key pathways affected included mitochondrial function, metabolism, remodeling, and stress responses.
- Upstream regulators like FOXO1/3, KLF15, and STAT3, known drivers of muscle atrophy, were identified.
Conclusions:
- Brain senescence is sufficient to cause sarcopenia-like transcriptomic remodeling in skeletal muscle.
- This establishes a brain-muscle aging axis, with the central nervous system acting as an upstream regulator of muscle aging.
- Targeting brain senescence may offer a novel strategy to combat systemic aging and muscle dysfunction.
Keywords:
Accelerated agingCell non-autonomous agingFOXO signalingFrailtyIrradiationMitochondrial dysfunctionSarcopeniaSenescenceSenescence-associated secretory phenotype (SASP)Skeletal muscle agingSystemic agingTranscriptomicsMore Related Videos
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