Duncan C J
Experientia. 1978 Dec 15;34(12):1531-5. doi: 10.1007/BF02034655.
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.
有人提出，各种肌肉疾病以及实验性诱导的肌肉损伤实例是由于肌浆中钙水平过高所致。当通过用A23187或咖啡因处理在两栖动物或哺乳动物肌肉中实验性地提高[Ca2+]i时，肌丝降解会迅速发生。这种快速作用表明存在一系列由[Ca2+]i升高刺激的蛋白水解活性。Ca2+可能直接或间接触发蛋白酶活性，或促进溶酶体酶的释放。营养不良肌肉中高[Ca2+]i被认为是图中总结的一系列事件的结果。针对如何最终控制[Ca2+]i的稳态位置以临床改善某些营养不良状况，提出了不同的方法建议。
