骨质疏松症线粒体代谢物传导机制
Mechanism of signal transduction of mitochondrial metabolites in osteoporosis
  
DOI:10.3969/j.issn.1006-7108.2025.05.018
中文关键词:  骨质疏松症  线粒体代谢物  传导机制
英文关键词:osteoporosis  mitochondrial metabolites  mechanism of signal transduction
基金项目:甘肃省联合科研基金项(24JRRA878);2025年省级人才项目重点一般项目(2025RCXM006);甘肃省自然科学基金项目(24JRRA1020);甘肃省科技计划项目重点研发计划国际科技合作类(25YFWA024)
作者单位
张浩令1,2,3 赵瑞4 齐雅茜4 Sandai Doblin2 王薇5 梁秋冬3* 宋志靖4,6* 1新乡医学院第一附属医院脊柱与创伤外科河南 新乡 453000 2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 3 甘肃中医药大学公共卫生学院甘肃 兰州 730000 4 甘肃中医药大学中医临床学院甘肃 兰州 730000 5 甘肃中医药大学针灸推拿学院甘肃 兰州 730000 6 敦煌医学与转化教育部重点实验室甘肃 兰州 730000 
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中文摘要:
      骨质疏松症(osteoporosis,OP)是一种常见的骨代谢紊乱疾病,其显著特征在于骨密度下降和骨组织微结构退化,导致骨骼脆性增加、骨折风险上升。本文提出一项理论:线粒体代谢物作为传导机制,在OP的发病过程中起着关键作用。线粒体不仅是细胞能量生成的核心枢纽,通过一系列复杂的生化反应生成大部分三磷酸腺苷,同时还作为信号转导的平台,通过调节钙离子流、生成活性氧自由基以及释放生物活性蛋白,与细胞内其他部分进行密切的信号交流。线粒体代谢产物作为二级信使,诱导深远的表观遗传变化,调控骨细胞的功能和骨代谢的动态平衡。本文揭示了线粒体代谢物在OP中的关键潜在作用,开辟了新的研究方向和治疗策略,对深入理解和有效应对OP的病理生理机制具有重要意义。
英文摘要:
      Osteoporosis is a prevalent disorder of bone metabolism, characterized by a marked reduction in bone mineral density and degradation of the bone tissue microarchitecture, leading to heightened bone fragility and an elevated risk of fractures. This paper proposes a theory that mitochondrial metabolites play a key role in the pathogenesis of OP as a conduction mechanism. Mitochondria, the center of primary energy production in the cell, generate the majority of adenosine triphosphate (ATP) through intricate biochemical processes. Additionally, they function as pivotal signal transduction platforms by modulating calcium ion flux, producing reactive oxygen species, and releasing bioactive proteins. These mitochondrial metabolites may act as secondary messengers, instigating significant (epigenetic) genetic modifications and regulating bone cell function and bone metabolic homeostasis. This hypothesis underscores the potential involvement of mitochondrial metabolites in osteoporosis, thereby paving a new avenue for research and therapeutic strategies. It holds substantial implications for a deeper understanding and effective intervention in the pathophysiological mechanisms underlying osteoporosis.
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