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Role of intracellular calcium in promoting muscle damage: A strategy for controlling the dystrophic condition

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Summary

It is suggested that various muscle diseases and examples of experimentally-induced muscle damage arise because of a high calcium level in the myoplasm. When [Ca2+]i is raised experimentally in amphibian or mammalian muscle by treatment with A23187 or caffeine, myofilament degradation follows quickly. Such a rapid action suggests the involvement of a sequence of proteolytic activity that is stimulated by a rise in [Ca2+]i. Ca2+ might either trigger protease activity directly or indirectly, or promote the release of lysosomal enzymes. A high [Ca2+]i in dystrophic muscle is believed to be the resultant of a sequence of events that is summarized in the figure. Suggestions are presented for different ways in which the steady-state position of [Ca2+]i might ultimately be controlled for the clinical amelioration of some dystrophic conditions.

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  1. Department of Zoology, University of Liverpool, P.O. Box 147, L69 3BX, Liverpool, UK

    C. J. Duncan

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This work was supported in part by the Muscular Dystrophy Group of Great Britain. I am grateful to Miss S. Scott for assistance in the preparation of the manuscript.

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Duncan, C.J. Role of intracellular calcium in promoting muscle damage: A strategy for controlling the dystrophic condition. Experientia 34, 1531–1535 (1978). https://doi.org/10.1007/BF02034655

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