肌肉运动与骨骼肌细胞的凋亡

Muscle exercise and apoptosis in the skeletal muscle

背景:不少医学研究表明,细胞凋亡能导致大量自由基增多、Ca2+浓度升高、线粒体膜电位下降引起运动能力的下降。因此,研究细胞凋亡与运动训练的关系意义重要。目的:总结与探索关于肌肉运动与骨骼肌细胞凋亡的相关问题。方法:计算机检索中国期刊全文数据(网址http://dlib.cnki.net/kns50/index.aspx)及PubMed数据库(网址http://www.ncbi.nlm.nih.gov/pubmed/)1990-01/2009-06期间的相关文章,检索词为"肌肉运动,骨骼肌细胞凋亡,muscle exercise,apoptosis in the skeletal muscle"。纳入与肌肉运动与骨骼肌细胞的凋亡研究现状与发展密切相关。①有关骨骼肌细胞凋亡的研究。②运动与骨骼肌细胞凋亡研究。③运动诱发骨骼肌细胞凋亡的基因调控研究。④骨骼肌细胞凋亡的分子机制研究。⑤同一领域选择近期发表或在权威杂志上发表的文章。排除重复性研究。结果与结论:运动后,正常肌肉中或是病理状态下的肌肉中骨骼肌细胞都会出现凋亡,凋亡的形态学表现与普通凋亡细胞相似,即核固缩、质膜发泡、细胞器紧缩,凋亡小体形成,其凋亡过程大致可分为3个阶段,即启始阶段、效应阶段和降解阶段。骨骼肌细胞凋亡的增加是导致运动性疲劳的重要原因。目前国内外对骨骼肌细胞凋亡的基因调控研究主要是从凋亡调控因子Bcl-2蛋白、肿瘤坏死因子α及死亡蛋白酶半胱氨酸天冬氨酸酶着手。bcl-2基因蛋白的抗凋亡作用主要是通过阻止线粒体通透性转换孔的开放,阻止线粒体释放促凋亡蛋白、防止线粒体膜脂质过氧化以及线粒体基质Ca2+释放实现的。肿瘤坏死因子家族在启动死亡因子及其受体途径中起重要作用,此途径的启动依赖于死亡配体与死亡受体相结合,激活半胱氨酸天冬氨酸酶,导致细胞凋亡。通过研究探索运动强度与骨骼肌细胞凋亡及坏死的界限关系,有利于在运动中认识运动性疲劳产生的机制及有效消除疲劳。

BACKGROUND： Studies have shown that cell apoptosis can increase free radical, elevate Ca2＋ concentration, and decrease mitochondrial membrane potential, ultimately reducing motor function. Therefore, understanding of relationship between apoptosis and exercise training is very important. OBJECTIVE： To summarize questions recording muscle exercise and apoptosis in skeletal muscle. METHODS： A computer-based online search of CNKI （http：//dlib.cnki.net/kns50/index.aspx）, and PubMed （http：//www.ncbi.nlm.nih.gov/pubmed/） was performed to collect articles published between January 1990 and June 2009 with the key words ＂muscle exercise, apoptosis in the skeletal muscle＂ in Chinese and English, respectively. Articles highly correlated with current status and development of muscle exercise and apoptosis in the skeletal muscle were included： ①studies on apoptosis in the skeletal muscle; ②studies concerning exercise and apoptosis in the skeletal muscle; ③studies involving gene regulation of exercise-induced apoptosis in the skeletal muscle; ④studies on molecular mechanism of apoptosis in the skeletal muscle; ⑤ studies published in latest journal or similar field. Repetitive studies were excluded. RESULTS AND CONCLUSION： After exercise, apoptosis occurs in normal muscle or muscle under pathologic state. The apoptosis of skeletal muscle cells is similar to common cell apoptosis, including karyopyknosis, plasma membrane vacuole, cell organ shrinking, and apoptotic body formation. The apoptosis process is classified into three stages： initial, effector, and degradation stages. The increased apoptosis in the skeletal muscle is the primary reason for sports fatigue. Currently, studies of gene regulation of apoptosis in the skeletal muscle focus on apoptosis regulatory factor Bcl-2 protein, tumor necrosis α and death protease cysteine aspartase. The bcl-2 inhibits opening of mitochondrial permeability transition pore, suppresses proapoptosis protein release from mitochondria, and prevents mitochondrial membrane lipid peroxidation and mitochondrial matrix Ca2＋ release to play anti-apoptotic effect. Tumor necrosis family plays an important role in initializing death factor and its receptor pathways, which depends on death ligand binding death receptor to activate cysteine aspartase and lead to cell apoptosis. The exploration of the relationship between exercise intensity and apoptosis and necrosis in skeletal muscle assists better understanding of the movement mechanism of exercise-induced fatigue and effectively reducing fatigue.