What is the clinical evidence from this study?

Study design: Review. Population: Sarcopenia. Intervention: Aging.

What question did this study set out to answer?

This review aims to explore the changes in the nucleus and its mechanosensory functions in aging muscle.

June 19, 2026NucleusOpen Access

The nucleus as a mechanobiological hub in muscle aging

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Key result

Aging alters the skeletal muscle matrix and cytoskeleton, impairing nuclear mechanosignaling to promote sarcopenia.

Why the study?

Aging causes sarcopenia through intrinsic cellular dysfunctions, and recent evidence indicates the nucleus acts as a mechanosensory organelle that may undergo age-related structural alterations compromising transcriptional control.

Design

Review

Authors

OEOsman EsenIstinye University EBEdmund BatteyUniversity of Copenhagen MSMatthew J. StroudKing's College London

Discussion

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Implication

Hypothesis-generating for sarcopenia therapies; leaves open translation to cardiovascular muscle outcomes.

Key Points

This review aims to explore the changes in the nucleus and its mechanosensory functions in aging muscle.
Analyzed changes in the extracellular matrix, cytoskeleton, LINC complex, and nuclear lamina in aged skeletal muscle.
Discussed the role of the nucleus in mechanotransduction and muscle fiber function.
Explored how aging impacts these cellular structures and their regulatory roles.
Elderly muscle shows altered nuclear morphology and decreased stiffness, leading to impaired mechanosignaling.
Nuclear envelope fragility was observed, compromising transcriptional control of muscle function.
Impaired mechanotransduction may contribute to the dysfunction observed in aging skeletal muscle.

Structured PICO

Population

Aged skeletal muscle (sarcopenia model)

This review highlights the role of the nucleus as a mechanosensory organelle and proposes that age-related structural changes in nuclear mechanosignaling contribute to sarcopenia.

Cite This Study

Esen et al. (2026) conducted a review in Sarcopenia. Aging was evaluated. Aging alters the extracellular matrix, cytoskeleton, LINC complex, and nuclear lamina in skeletal muscle, leading to impaired nuclear mechanosignaling and contributing to sarcopenia.

synapsesocial.com/papers/6a35982fdd3be7785e70ed44 https://doi.org/10.1080/19491034.2026.2688584

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The nucleus as a mechanobiological hub in muscle aging

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

The nucleus as a mechanobiological hub in muscle aging

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Also Consider