Institute of Biomedical Problems RAS, 123007 Moscow, Russia.
Int J Mol Sci. 2022 Jun 22;23(13):6937. doi: 10.3390/ijms23136937.
A decrease in skeletal muscle contractile activity or its complete cessation (muscle unloading or disuse) leads to muscle fibers' atrophy and to alterations in muscle performance. These changes negatively affect the quality of life of people who, for one reason or another, are forced to face a limitation of physical activity. One of the key regulatory events leading to the muscle disuse-induced changes is an impairment of calcium homeostasis, which leads to the excessive accumulation of calcium ions in the sarcoplasm. This review aimed to analyze the triggering mechanisms of calcium homeostasis impairment (including those associated with the accumulation of high-energy phosphates) under various types of muscle unloading. Here we proposed a hypothesis about the regulatory mechanisms of SERCA and IP3 receptors activity during muscle unloading, and about the contribution of these mechanisms to the excessive calcium ion myoplasmic accumulation and gene transcription regulation via excitation-transcription coupling.
骨骼肌收缩活动减少或完全停止(肌肉失用或废用)会导致肌肉纤维萎缩,并改变肌肉性能。这些变化会降低因某种原因被迫限制体力活动的人的生活质量。导致肌肉废用引起的变化的关键调节事件之一是钙稳态的损害,这导致肌浆中钙离子的过度积累。本综述旨在分析各种类型的肌肉失用下钙稳态损害的触发机制(包括与高能磷酸化合物积累相关的机制)。在这里,我们提出了一个关于肌肉失用期间 SERCA 和 IP3 受体活性的调节机制的假设,以及这些机制对过度钙离子肌浆内积累和基因转录调控通过兴奋-转录偶联的贡献。