一个突破性的研究发现，干细胞可以通过一种目前用于治疗骨质疏松症患者药物来防止老化的影响。
来自谢菲尔德大学的科学家发现了一种药物唑来膦酸通过减少DNA损伤能够延长间充质干细胞的寿命。
DNA损伤是最重要的一种老化机制，由此干细胞会失去维护和修复组织的能力。
开创性的研究显示，药物保护干细胞免受DNA损伤会提高它们的生存能力并保持其功能性。
新陈代谢学部的Ilaria Bellantuono教授说：“这种药物提高了骨骼干细胞中老化DNA损伤的修复。它也可能在其他干细胞中作用。”
“这种药被证明可延迟骨质疏松症患者死亡，但直到现在我们也不知道为什么。这些发现提供了一个解释，就是为什么它可能帮助人们活得更久。”
“现在我们想了解使用该药物是否可以延迟或恢复老年人干细胞的老化状况，并且可以提高一些组织器官的维护，如心脏、肌肉和免疫细胞，让它们保持长久健康。”
“我们想了解例如当老年癌症患者接受放射治疗时是否可以提高干细胞的能力来修复这些损伤组织。”
大约有50%的超过75岁的老人同时患有三种或更多种的疾病，如心血管疾病、感染、肌肉无力和骨质疏松症等。在未来，希望这种药物可以用于治疗或延缓以及预防这些疾病的发病而不是联合用药。
Bellantuono博士补充说：“我们希望通过减少多种年龄相关疾病风险的这项研究能更好的治愈癌症病人，并且使老年人保持更持久的健康时间。”
doi:10.1002/stem.2255
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ZoledronateAttenuates Accumulation of DNA Damage in Mesenchymal Stem Cells and Protectstheir Function
Juhi Misra1,Sindhu T. Mohanty1, Sanjeev Madan2, James A. Fernandes2, F. Hal Ebetino3,4, R.Graham, G. Russell1,5 andIlaria Bellantuono1,*
AbstractMesenchymal stem cells (MSC) undergo a decline in function following ex vivoexpansion and exposure to irradiation. This has been associated withaccumulation of DNA damage and has important implications for tissueengineering approaches or in patients receiving radiotherapy. Thereforeinterventions, which limit accumulation of DNA damage in MSC, are of clinicalsignificance. We were intrigued by findings showing that zoledronate, ananti-resorptive nitrogen containing bisphosphonate, significantly extendedsurvival in patients affected by osteoporosis. The effect was too large to besimply due to the prevention of fractures. Moreover, in combination withstatins it extended the lifespan in a mouse model of Hutchinson GilfordProgeria Syndrome. Therefore, we asked whether zoledronate was able to extendthe lifespan of human MSC and whether this was due to reduced accumulation ofDNA damage, one of the important mechanisms of aging. Here we show that thiswas the case both following expansion and irradiation, preserving their abilityto proliferate and differentiate in vitro. In addition, administration ofzoledronate prior to irradiation protected the survival of mesenchymalprogenitors in mice. Through mechanistic studies we were able to show that inhibitionof mTOR signalling, a pathway involved in longevity and cancer, was responsiblefor these effects. Our data open up new opportunities to protect MSC from theside effects of radiotherapy in cancer patients and during ex vivo expansionfor regenerative medicine approaches. Given that zoledronate is already inclinical use with a good safety profile, these opportunities can be readilytranslated for patient benefit. This article is protected by copyright. Allrights reserved.
来源：生物谷
