外泌体非编码RNA调控骨折愈合机理的研究进展△
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苏友祥,硕士研究生,研究方向:脊柱脊髓损伤、骨质疏松、脊柱退行性疾病相关研究,(电话)13708939703,(电子信箱)540115112@qq.com

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R318

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山东省自然科学基金项目(编号:ZR2019MH044);徐展望山东省名老中医药专家传承工作室建设项目(编号:山东省卫生健康委员会鲁卫函[2019]92 号)


Research progress on exosome non- coding RNA in regulation mechanism of fracture healing
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    摘要:

    外泌体是细胞旁分泌的重要组成部分,它们参与细胞因子、mRNAs、miRNAs 和蛋白质等生化物质的转运,并通过遗传物质的转移在细胞间通讯中发挥重要作用。非编码RNA 主要包括微小RNA、长链非编码RNA 和环状RNA,可以被外泌体选择性的摄取并递送到受体细胞,从而调节受体细胞的生理活动和功能。骨折是人类常见的器官创伤性损伤,其愈合过程由早期炎症反应驱动,伴随着各种生物活动,利用内源性再生潜力恢复原始骨结构。近年来,越来越多的研究开始关注外泌体ncRNA 在骨折愈合过程中的调控机理,本文通过回顾相关研究成果,探索外泌体ncRNA 在骨折愈合中的详细作用机制。

    Abstract:

    Exosome, as an important component of paracellular secretion, are involved in the transport of biochemical substances suchas cytokines, mRNAs, miRNAs, and protein, and play an important role in intercellular communication through the transfer of genetic mate-rial. Non-coding RNA (ncRNA), mainly including microRNA, long-chain non-coding RNA and cyclic RNA, which can be selectively in-gested and delivered by the exosome to the receptor cells, thereby regulating the physiological activities and functions of the receptor cells.Fracture is a common traumatic consequence in humans, and its fracture healing process is driven by the early inflammatory response, ac-companied by a variety of biological activities, using the endogenous regeneration potential to restore the original bone structure. In recentyears, more and more attention has been paid to the regulatory mechanism of exosome ncRNA in fracture healing. By reviewing the researchresults in this field, we explored the detailed mechanism of exosome ncRNA in fracture healing.

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苏友祥,李志超,管华鹏,等. 外泌体非编码RNA调控骨折愈合机理的研究进展△[J]. 中国矫形外科杂志, 2023, 31 (24): 2260-2263. DOI:10.3977/j. issn.1005-8478.2023.24.10.
SU You- xiang, LI Zhichao, GUAN Hua-peng, et al. Research progress on exosome non- coding RNA in regulation mechanism of fracture healing[J]. Orthopedic Journal of China , 2023, 31 (24): 2260-2263. DOI:10.3977/j. issn.1005-8478.2023.24.10.

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  • 收稿日期:2022-10-10
  • 最后修改日期:2023-04-07
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  • 在线发布日期: 2023-12-28
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