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27 - Cell Death Regulation in Muscle

from Part II - Cell Death in Tissues and Organs

Published online by Cambridge University Press:  07 September 2011

Douglas R. Green
Affiliation:
St. Jude Children's Research Hospital, Memphis, Tennessee
Ayesha Saleem
Affiliation:
York University, Canada
Lawrence Kazak
Affiliation:
York University, Canada
Michael O'Leary
Affiliation:
York University, Canada
David A. Hood
Affiliation:
York University, Canada
John C. Reed
Affiliation:
Sanford-Burnham Medical Research Institute, La Jolla, California
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Summary

Introduction To Muscle

Skeletal muscle constitutes ~40% of total body weight, and its primary function is to provide force and energy for locomotion, breathing, and postural support. It can also act as a source of heat production during cold-induced stress or exercise. Skeletal muscle is a highly adaptable tissue that exhibits a remarkable range of plasticity in response to different stimuli. It possesses distinctive structural and biochemical properties that distinguish it from all other tissues. There is a significant variation in size, type, and shape of skeletal muscles within the body. However, the underlying morphological structure remains the same. Common to all skeletal muscle is the presence of multiple myonuclei per cell, the innervation of several cells by single α-motor neurons, and the presence of ligaments and tendons.

Type
Chapter
Information
Apoptosis
Physiology and Pathology
, pp. 313 - 322
Publisher: Cambridge University Press
Print publication year: 2011

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References

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Adhihetty, P.J., Ljubicic, V., and Hood, D.A.. Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle. Am J Physiol Endocrinol Metab. 292 (2007), E748–55.
Allen, D.L., Roy, R.R., and Edgerton, V.R.. Myonuclear domains in muscle adaptation and disease. Muscle Nerve. 22 (1999), 1350–60.
Bruusgaard, J.C., Johansen, I.B., Egner, I.M., Rana, Z.A., Gundersen, K.. Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proc Natl Acad Sci U S A. 107(34) (2010), 151116.
Cadenas, E. and Davies, K.J.. Mitochondrial free radical generation, oxidative stress, and aging. Free Radic Biol Med. 29 (2000), 222–30.
Chabi, B., Ljubicic, V., Menzies, K.J., Huang, J.H., Saleem, A., and Hood, D.A.. Mitochondrial function and apoptotic susceptibility in aging skeletal muscle. Aging Cell. 7 (2008), 2–12.
Chipuk, J.E. and Green, D.R.. How do BCL-2 proteins induce mitochondrial outer membrane permeabilization? Trends Cell Biol. 18 (2008), 157–64.
Dirks, A.J., Hofer, T., Marzetti, E., Pahor, M., and Leeuwenburgh, C.. Mitochondrial DNA mutations, energy metabolism and apoptosis in aging muscle. Ageing Res Rev. 5 (2006), 179–95.
Hood, D.A., Irrcher, I., Ljubicic, V., and Joseph, A.M.. Coordination of metabolic plasticity in skeletal muscle. J Exp Biol. 209 (2006), 2265–75.
Scime, A. and Rudnicki, M.A.. Anabolic potential and regulation of the skeletal muscle satellite cell populations. Curr Opin Clin Nutr Metab Care. 9 (2006), 214–19.
Siu, P.M., Bryner, R.W., Martyn, J.K., and Alway, S.E.. Apoptotic adaptations from exercise training in skeletal and cardiac muscles. FASEB J. 18 (2004), 1150–2.

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