title: Role of intracellular calcium in promoting muscle damage: a strategy for controlling the dystrophic condition.
abstract: 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 mammaliam 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.
mesh_terms: D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D008274:Magnesium / Q000494:pharmacology; D009135:Muscular Diseases / Q000378:metabolism* / Q000473:pathology; D009136:Muscular Dystrophies / Q000378:metabolism* / Q000473:pathology; D009712:Nucleotides, Cyclic / Q000502:physiology; D009994:Osmolar Concentration; D010447:Peptide Hydrolases / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism
chemical_list: D009712:Nucleotides, Cyclic; D000001:Calcimycin; D002110:Caffeine; D010447:Peptide Hydrolases; D008274:Magnesium; D002118:Calcium