运动干预对骨Ⅰ型胶原蛋白含量的影响

Effects of Exercise Intervention on Type Ⅰ Collagen Content in Bone

骨作为机内的重要组织器官,相关信号途径或关键分子通过调控成骨细胞(Osteoblast,OB)合成Ⅰ型胶原蛋白,为钙、磷等矿物质沉积提供载体,使得骨量增加,改善骨质疏松。而运动作为影响骨代谢的重要手段,其促进OB分化及骨形成,使得骨中Ⅰ型胶原蛋白及骨密度(Bone mineral density,BMD)增加。但目前有关运动影响骨中Ⅰ型胶原蛋白合成的研究较少,其分子机制尚不明确。TGF-β/BMPs、Notch、Hedgehog、miRNAs等途径或关键因子在调控OB分化产生和Ⅰ型胶原蛋白合成均具有重要作用。虽然,运动可显著激活或上调以上信号途径或关键因子表达,但目前有关运动通过以上信号途径或关键因子进而影响骨中Ⅰ型胶原蛋白表达,并改善骨质疏松的相关研究尚未见报道。通过分析国内外相关研究,对Ⅰ型胶原蛋白在改善骨质疏松中的作用和运动影响骨中Ⅰ型胶原蛋白合成的作用及分子机制进行综述。

Bone as an important organ,the osteoblast,which regulated by signal pathways or key molecules,could synthesis typeⅠcollagen and provide carrier for calcium,phosphorus,promote bone formation and improve osteoporosis. Exercise as an important ways of improving bone metabolism,which can promote OB differentiation and bone formation,increased the typeⅠcollagen and bone mass in bone. However,there are few studies on the effect of exercise on typeⅠcollagen in bone,and its molecular mechanism is also not clear. TGF-β/BMPs,Notch,Hedgehog,miRNAs and other pathways or key factors play important role in the differentiation of OB and synthesis of type Ⅰ collagen. Exercise can significantly activate or upregulate the above pathways or key factor expression. However,exercise affect the expression of typeⅠcollagen through above signal pathways or key factors has not been reported. In this study,we reviewed the effects of typeⅠcollagen on osteoporosis and exercise on the expression of typeⅠcollagen in bone and the molecular mechanism.