Aging alters the extracellular matrix, cytoskeleton, LINC complex, and nuclear lamina in skeletal muscle, leading to impaired nuclear mechanosignaling and contributing to sarcopenia.
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.
Aging leads to a progressive loss of muscle mass and strength, termed sarcopenia, which is accelerated by inactivity and exacerbated by intrinsic cellular and molecular dysfunctions within the muscle fiber. Central to these changes is mechanotransduction, the process by which mechanical stimuli are converted into biochemical cues critical for protein synthesis, cytoskeletal remodeling, calcium signaling, and metabolism. Recent evidence highlights the nucleus as a key mechanosensory organelle in skeletal muscle. Forces transmitted from the extracellular matrix (ECM) through the cytoskeleton reach the nuclear envelope, where the Linker of Nucleoskeleton and Cytoskeleton (LINC) complex and nuclear lamina convert physical stress into gene-regulatory events. Aging may alter these structures, producing changes in nuclear morphology, decreased stiffness, envelope fragility, and compromised transcriptional control. This review examines how the ECM, cytoskeleton, LINC complex, and nuclear lamina change in aged skeletal muscle, proposing that impaired nuclear mechanosignaling contributes to muscle fiber dysfunction during physiological aging.
Esen et al. (Thu,) 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.
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