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当骨在不应该形成的地方形成时:肌肉损伤和疾病中的异型骨化

Anthony Facchin¹, Sophie Lemaire², Li Gang Toner²

¹Centre Hospitalier Universitaire de Québec-Université Laval Research Center (CHUQ-CHUL), Axe Neurosciences, Université Laval, Quebec City, QC G1V 4G2, Canada.

International journal of molecular sciences

|August 14, 2025

概括

异型骨化 (HO) 是软组织中的骨质形成,通常是在神经受伤后发生的. 这篇评论详细介绍了炎症,原生细胞和这种疾病的治疗方法.

科学领域:

病理学病理学病理学
细胞生物学细胞生物学
再生医学是一种再生医学.

背景情况:

异型骨化 (HO) 是软组织中的异常骨生长,经常发生在创伤,手术或遗传疾病后.
神经性HO (NHO) 是一种特定类型的HO,与中枢神经系统损伤有关.
了解HO机制对于开发有效治疗方法至关重要.

研究的目的:

审查HO背后的细胞和分子机制.
专注于炎症和原始细胞重编程在HO病变发生中的作用.
讨论当前和新的HO治疗策略.

主要方法:

对HO的细胞和分子机制的文献综述.
对炎症途径的分析,特别是来自M1巨细胞的细胞因子.
检查原生细胞 (纤维-基原生细胞 - - FAPs) 的分化和重编程.
审查导致的因素,如缺氧,BMP信号和机械传导.
在NHO中评估神经内分泌媒介作用.
评估当前治疗疗效和局限性.

主要成果:

HO是由持续的炎症驱动的,M1巨细胞释放骨诱导性细胞因子.
这些细胞因子诱导纤维基原始细胞 (FAPs) 分化为骨质母细胞,导致宫外矿化.
缺氧,BMP信号传递和机械传导进一步促进细胞外基质重塑和FAP骨质性重编程.
神经内分泌介质通过影响炎症和原生细胞命运来加剧NHO.
目前的治疗方法 (NSAIDs,辐射,手术) 显示出有限的疗效,并带有风险.

结论:

炎症和祖细胞重编程是HO的关键驱动因素.
神经内分泌因素在NHO发展中发挥着重要作用.
需要针对炎症,神经信号传递和代谢的新疗法.
需要更有效的预防和缓解HO的策略.

关键词:

细胞外矩阵是细胞外矩阵.纤维基原体细胞原始细胞.不同类型的骨化异型化.淋巴细胞淋巴细胞.巨细胞是一个巨细胞.代谢代谢代谢代谢神经炎症是一种神经炎症.这是骨肌肉的骨架肌肉.

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