咖啡因作为研究人类骨骼肌肌浆网和细胞内钙动力学的工具。

IF 1.8 3区 生物学 Q4 CELL BIOLOGY
Carlo Reggiani
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引用次数: 14

摘要

咖啡因因其提高认知能力和身体表现的能力而在世界范围内广泛使用。然而,咖啡因对人体的作用并不依赖于对肌肉的直接作用。实际上,咖啡因对骨骼肌的作用是在毫摩尔浓度下发生的,这远远高于经常饮用咖啡或类似饮料后所达到的微摩尔浓度,接近致命浓度。在毫摩尔浓度下,咖啡因对肌浆网(SR)产生强大的影响,通过ryanodine受体激活钙的释放,并可能抑制钙的再摄取。因此,咖啡因已成为研究SR功能和诊断SR相关肌肉疾病的有价值的工具。本文简要介绍了咖啡因对肌浆网的作用和作用机制,并重点介绍了咖啡因在生理和病理状态下对人体肌纤维细胞内钙动力学的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Caffeine as a tool to investigate sarcoplasmic reticulum and intracellular calcium dynamics in human skeletal muscles.

Caffeine is worldwide used for its power to increase cognitive and physical performance. The ergogenic effects of caffeine, however, do not depend on a direct action on muscles. Actually, the actions of caffeine on skeletal muscles, take place at millimolar concentrations which are far above the micromolar level reached after a regular consumption of coffee or similar drinks, and close to a lethal concentration. At millimolar concentrations caffeine exerts a powerful effect on sarcoplasmic reticulum (SR) activating the release of calcium via ryanodine receptors and, possibly, inhibiting calcium reuptake. For this reason caffeine has become a valuable tool for studying SR function and for diagnostics of SR related muscle disorders. This review aims to briefly describe the effects and the mechanism of action of caffeine on sarcoplasmic reticulum and to focus on its use to study intracellular calcium dynamics in human muscle fibers in physiological and pathological conditions.

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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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