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体外实验表明，适度低氧下MSCs的生长和存活能力更好，产生集落形成单位的能力显著增高，且干细胞标志性基因表达水平更高[7]。氧浓度可以影响MSCs向成骨、成软骨、成脂的分化倾向，低氧能提高特异性受体和配体相结合所介导的迁移。低氧诱导因子1信号通路[8]在MSCs对缺氧反应的分子机制中占重要地位。
对缺氧反应的分子机制本实验主要研究了CMS患者骨髓MSC的形态、表型、传代能力、生长曲线及扩增能力等特征，其结果为CMS的研究提供了重要信息。但研究报道例数尚较少，结论还需要深入的体内实验及分子生物学研究支持。
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