Nuclear apoptosis and sarcopenia

Stephen Alway, Parco M. Siu

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Apoptosis is a well-conserve cellular disassembly process, which has been implicated in a variety of diseases. Unlike cells with a single nucleus, apoptotic signaling can target individual nuclei in multi-nucleated skeletal muscle cells without necessarily eliminating the entire cell (muscle fiber). This targeted apoptosis or nuclear apoptosis appears to have a role in regulating aging-induced muscle loss (sarcopenia) by reducing the myofiber volume (i.e. cytoplasm) that can be supported in a single muscle fibre. Recent investigations indicate that apoptotic signaling in aged skeletal muscles occurs through three apoptotic pathways. The intrinsic or mitochondria apoptotic pathway has been most widely studied in muscle. Mitochondria dysfunction and increased mitochondria permeability lead to activation of cysteine-aspartic acid proteases (caspases) and eventually DNA fragmentation in sarcopenia. The death receptor (extrinsic) apoptotic pathway has been strongly implicated in sarcopenia and other conditions of muscle loss with aging or disuse. TNF-α is thought to initiate apoptotic signaling via the death receptor, and this can proceed to activate the effort proteases (e.g., caspase 3) independent from mitochondria signaling. Nevertheless, there is some cross-talk between the intrinsic and the extrinsic apoptotic pathways. Finally, a few studies have shown data to suggest that the endoplasmic reticulum-stress apoptotic pathway may also have a role in sarcopenia, although the importance of this pathway relative to the other two pathways is less clear. Both myonuclei and satellite cells appear to be susceptible to nuclear apoptosis in sarcopenia.

Original languageEnglish (US)
Title of host publicationSarcopenia - Age-Related Muscle Wasting and Weakness
Subtitle of host publicationMechanisms and Treatments
PublisherSpringer Netherlands
Pages173-206
Number of pages34
Volume9789048197132
ISBN (Electronic)9789048197132
ISBN (Print)9789048197125
DOIs
StatePublished - Jan 1 2011
Externally publishedYes

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Sarcopenia
Apoptosis
Mitochondria
Aspartic Acid Proteases
Muscles
Death Domain Receptors
Muscle Cells
Skeletal Muscle
Endoplasmic Reticulum Stress
Cysteine Proteases
DNA Fragmentation
Cysteine
Permeability
Cytoplasm

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Alway, S., & Siu, P. M. (2011). Nuclear apoptosis and sarcopenia. In Sarcopenia - Age-Related Muscle Wasting and Weakness: Mechanisms and Treatments (Vol. 9789048197132, pp. 173-206). Springer Netherlands. https://doi.org/10.1007/978-90-481-9713-2_9

Nuclear apoptosis and sarcopenia. / Alway, Stephen; Siu, Parco M.

Sarcopenia - Age-Related Muscle Wasting and Weakness: Mechanisms and Treatments. Vol. 9789048197132 Springer Netherlands, 2011. p. 173-206.

Research output: Chapter in Book/Report/Conference proceedingChapter

Alway, S & Siu, PM 2011, Nuclear apoptosis and sarcopenia. in Sarcopenia - Age-Related Muscle Wasting and Weakness: Mechanisms and Treatments. vol. 9789048197132, Springer Netherlands, pp. 173-206. https://doi.org/10.1007/978-90-481-9713-2_9
Alway S, Siu PM. Nuclear apoptosis and sarcopenia. In Sarcopenia - Age-Related Muscle Wasting and Weakness: Mechanisms and Treatments. Vol. 9789048197132. Springer Netherlands. 2011. p. 173-206 https://doi.org/10.1007/978-90-481-9713-2_9
Alway, Stephen ; Siu, Parco M. / Nuclear apoptosis and sarcopenia. Sarcopenia - Age-Related Muscle Wasting and Weakness: Mechanisms and Treatments. Vol. 9789048197132 Springer Netherlands, 2011. pp. 173-206
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