细胞衰老及其驱动基因与骨质疏松症研究进展
Research progress of cell senescence and its driving genes and osteoporosis
  
DOI:10.3969/j.issn.1006-7108.2025.02.010
中文关键词:  细胞衰老  驱动基因  成骨细胞  破骨细胞  骨髓间充质干细胞  骨质疏松症
英文关键词:cell senescence  driver gene  osteoblast  osteoclast  bone marrow mesenchymal stem cells  osteoporosis
基金项目:国家自然科学基金(81960877);甘肃省高等学校创新基金(2023A-088;2022A-0674)敦煌医学与转化教育部重点实验室开放基金项目(DHYX20-16;DHYX21-01;DHYX2021-07;DHYX22-05);甘肃省自然基金(21JR1RA267;22JR5RA582;24JRRA1020);甘肃省教育科技创新项目(2022A-067);甘肃省科研联合基金一般项目(24JRRA878);甘肃省重点人才项目(2025RCXM006)
作者单位
王薇1 杨钰婷1 白金霞1 赵瑞2 齐雅茜2 雷新宇2 张忠文3 张浩令4* 宋志靖2,5* 1.甘肃中医药大学针灸推拿学院甘肃 兰州 730000 2.甘肃中医药大学中医临床学院甘肃 兰州 730000 3.甘肃中医药大学公共卫生学院甘肃 兰州 730000 4.马来西亚理科大学高级医学和牙科研究所马来西亚 槟城13200 5.教育部敦煌医学与转化重点实验室甘肃 兰州 730000 
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中文摘要:
      骨质疏松症(osteoporosis,OP)是一种代谢性疾病,以骨量减少和骨骼脆性增加为其特征。随着中国人口老龄化程度的不断加剧,OP的发病率也在上升。OP的发病原因多种多样,其中主要包括更年期、生理衰老和药物不良反应。随着时间的推移,衰老相关细胞在组织中逐渐积累,与整个生物体的退化和老化紧密相关。近年来的研究表明,细胞衰老在维持OP中的细胞稳态和器官功能起着至关重要的作用。其次,许多蛋白质被鉴定为生物标志物和导致细胞衰老的因果驱动因子。因此,深入了解细胞衰老驱动基因的发生机制、调控方式以及其与OP之间的关系变得尤为重要。因此,本文重点探讨了细胞衰老驱动基因以及衰老相关分泌表型(senescence-associated secretory phenotype,SASP)在OP中对成骨细胞、破骨细胞和骨髓间充质干细胞的作用机制的研究进展。
英文摘要:
      Osteoporosis (OP) is a metabolic disorder characterized by reduced bone mass and heightened bone fragility. As the Chinese population continues to age, the prevalence of OP is on the rise. OP has multifaceted etiologies, including menopause, natural aging processes, and adverse reactions to medications. Over time, cells associated with aging progressively accumulate in tissues and are intimately linked to overall organismal degeneration and aging. Recent investigations have demonstrated that cellular senescence assumes a pivotal role in upholding cellular homeostasis and organ function in OP. Furthermore, numerous proteins have been identified as biomarkers and causal drivers of cellular aging. Consequently, comprehending the mechanisms of cell senescence driver genes, their regulatory modes, and their associations with OP becomes particularly vital. Therefore, this paper focuses on the research progress of senescence driver genes and the mechanism of senescence associated secretory phenotype (SASP) on osteoblasts, osteoclasts and bone marrow mesenchymal stem cells (BMSCS) in OP.
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