著者

Jun Tanihata Shin’ichi Takeda

出版者

一般社団法人日本体力医学会

雑誌

The Journal of Physical Fitness and Sports Medicine (ISSN:21868131)

巻号頁・発行日

vol.5, no.4, pp.309-312, 2016-09-25 (Released:2016-10-03)

参考文献数

38

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Duchenne muscular dystrophy (DMD) is a life-limiting X-linked genetic disorder caused by a lack of the membrane-associated protein dystrophin. The absence of dystrophin increases the susceptibility of muscle fibers to damage. Repeated damage results in ineffective muscle repair and the development of pseudo-hypertrophied muscles; these bulky muscles are weak despite their size. The mechanisms underlying the functional impairments in dystrophic muscle have not yet been fully determined. However, several recent studies indicate that elevated intracellular Ca2+ homeostasis is a cause or facilitator of the development of muscle weakness in DMD. This review focuses on abnormalities of Ca2+ homeostasis and the possibilities for treatment by counteracting the Ca2+ dysregulation.