Nishikawa Hiroki, Fukunishi Shinya, Asai Akira, Yokohama Keisuke, Nishiguchi Shuhei, Higuchi Kazuhide
The Second Department of Internal Medicine, Osaka Medical and Pharmaceutical University, Takatsuki, Osaka 569‑8686, Japan.
Department of Internal Medicine, Kano General Hospital, Osaka 531‑0041, Japan.
Int J Mol Med. 2021 Aug;48(2). doi: 10.3892/ijmm.2021.4989. Epub 2021 Jun 29.
Aging causes skeletal muscle atrophy, and myofiber loss can be a critical component of this process. In 1989, Rosenberg emphasized the importance of the loss of skeletal muscle mass that occurs with aging and coined the term 'sarcopenia'. Since then, sarcopenia has attracted considerable attention due to the aging population in developed countries. The presence of sarcopenia is closely related to staggering, falls and even frailty in the elderly, which in turn leads to the need for nursing care. Sarcopenia is often associated with a poor prognosis in the elderly. Therefore, it is crucial to investigate the causes and pathogenesis of sarcopenia, and to develop and introduce interventional strategies in line with these causes and pathogenesis. Sarcopenia can be a primary component of physical frailty. The association between sarcopenia, frailty and locomotive syndrome is complex; however, sarcopenia is a muscle‑specific concept that is relatively easy to approach in research. In the elderly, a lack of exercise, malnutrition and hormonal changes lead to neuromuscular junction insufficiency, impaired capillary blood flow, reduced repair and regeneration capacity due to a decrease in the number of muscle satellite cells, the infiltration of inflammatory cells and oxidative stress, resulting in muscle protein degradation exceeding synthesis. In addition, mitochondrial dysfunction causes metabolic abnormalities, such as insulin resistance, which may lead to quantitative and qualitative abnormalities in skeletal muscle, resulting in sarcopenia. The present review article focuses on age‑related primary sarcopenia and outlines its pathogenesis and mechanisms.
衰老会导致骨骼肌萎缩,肌纤维丢失可能是这一过程的关键组成部分。1989年,罗森伯格强调了衰老过程中发生的骨骼肌质量丢失的重要性,并创造了“肌肉减少症”一词。从那时起,由于发达国家人口老龄化,肌肉减少症受到了相当多的关注。肌肉减少症的存在与老年人步履蹒跚、跌倒甚至虚弱密切相关,进而导致需要护理。肌肉减少症通常与老年人预后不良相关。因此,研究肌肉减少症的病因和发病机制,并根据这些病因和发病机制制定和引入干预策略至关重要。肌肉减少症可能是身体虚弱的主要组成部分。肌肉减少症、虚弱和运动机能减退综合征之间的关联很复杂;然而,肌肉减少症是一个特定于肌肉的概念,在研究中相对容易研究。在老年人中,缺乏运动、营养不良和激素变化会导致神经肌肉接头功能不全、毛细血管血流受损、由于肌肉卫星细胞数量减少、炎症细胞浸润和氧化应激导致的修复和再生能力降低,从而导致肌肉蛋白降解超过合成。此外,线粒体功能障碍会导致代谢异常,如胰岛素抵抗,这可能导致骨骼肌的数量和质量异常,从而导致肌肉减少症。本综述文章重点关注与年龄相关的原发性肌肉减少症,并概述其发病机制。