Aging preserves mTORC1 but weakens JNK-SMAD2L stretch sensitivity in isolated mouse muscle
In isolated extensor digitorum longus muscles from female mice, passive stretch raised mTORC1-related phosphorylation in both adult and old muscle with no significant age difference, while JNK and SMAD2-L activation was weaker in old muscle. [1]
Automatic summary · not editorially reviewed
The key findings
EDL muscles from adult (16 weeks) and old (24 months) female mice underwent a standardized passive stretch protocol, with contralateral muscles as controls. [1]
Passive stretch significantly increased mTORC1-related phosphorylation in both age groups, with no significant differences between them. [1]
The magnitude of JNK and SMAD2-L signaling activation was attenuated in old muscles. [1]
The source at a glance
- Study type / format
- Ex vivo animal study (abstract)
- Population / context
- Isolated extensor digitorum longus muscles from adult (16 weeks) and old (24 months) female mice.
- Summary based on
- Study abstract
- Original publication
- August 4, 2026
Stretch test in adult and old mouse EDL muscle
The study asked whether aging changes how key anabolic signaling pathways respond to mechanical tension in skeletal muscle. Using an ex vivo model, the researchers took extensor digitorum longus (EDL) muscles from adult female mice at 16 weeks and old female mice at 24 months. Muscles underwent a standardized passive stretch protocol, and the contralateral muscles served as controls. During recovery, phosphorylation of proteins linked to downstream mTORC1 and JNK-SMAD2-L signaling was measured by immunoblotting.
Supporting source [1]
mTORC1 response preserved, JNK-SMAD2L weaker in old muscle
Passive stretch significantly increased phosphorylation of mTORC1-related proteins (mTOR, p70S6K, rpS6 and 4E-BP1) in both adult and old muscles, with no significant differences between age groups. The authors read this as preserved mTORC1 signaling sensitivity to mechanical tension with aging. In contrast, the magnitude of JNK and SMAD2-L signaling activation was attenuated in old muscles. The authors describe this as reduced mechanosensitivity of JNK-SMAD2L signaling in aged muscle.
Supporting source [1]
Divergent signaling and limits of an isolated-muscle abstract
The authors conclude that mechanosensitive anabolic signaling is differentially affected by aging: the intrinsic capacity for mTORC1 activation appears preserved, while tension-sensitive transcriptional pathways may be selectively impaired, potentially constraining muscle remodeling despite preserved translational signaling. They suggest age-related deficits seen in vivo may partly arise from systemic influences rather than intrinsic defects in mTORC1 mechanotransduction. These are interpretations from an ex vivo mouse model; the abstract reports no sample sizes per group, no effect sizes and no full-text details, and the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from an ex vivo mouse EDL model, not from human muscle or in vivo outcomes. The abstract reports no group sizes, effect sizes or statistical details, and the proposed systemic explanation is an interpretation, not a tested result.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Kristiansen JB, Andresen J, Jakobsgaard JE, Vissing K. · europepmc.org · August 4, 2026