乳酰化在老年性骨质疏松症中的作用机制探究

作者	单位	邮编
白磊^*	1天津中医药大学,天津,301600 2天津大学天津医院,天津,300200 3天津市骨科研究所,天津,300041 4天津市骨科生物力学与医学工程重点实验室,天津,300041	300041
贾敬坤	2天津大学天津医院,天津,300200 3天津市骨科研究所,天津,300041 4天津市骨科生物力学与医学工程重点实验室,天津,300041	300041
马剑雄	2天津大学天津医院,天津,300200 3天津市骨科研究所,天津,300041 4天津市骨科生物力学与医学工程重点实验室,天津,300041	300041
马信龙^*	2天津大学天津医院,天津,300200 3天津市骨科研究所,天津,300041 4天津市骨科生物力学与医学工程重点实验室,天津,300041	300041

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中文摘要:

老年性骨质疏松症是严重危害老年人群健康的常见退行性骨骼疾病，其以骨量进行性减少、骨组织微结构破坏及骨强度下降为主要病理特征，其核心危害是显著升高脆性骨折发生风险，进而诱发多种并发症。随着全球人口老龄化进程加剧及现代生活方式转变，该病发病率持续攀升，不仅损害患者躯体健康与自主生活能力、降低生存质量，更给医疗保健体系带来沉重疾病负担与经济压力。乳酰化作为近年备受关注的新型翻译后修饰方式，在细胞信号转导、代谢重编程、免疫功能调控等多个生物学领域的关键调控作用已逐步阐明，尤其在骨代谢稳态维持、骨相关细胞功能调控等方面展现出重要潜在价值。本文构建了“乳酰化－骨细胞功能－骨代谢微环境－信号通路”的系统性调控框架，整合了乳酰化对成骨、破骨及骨髓间充质干细胞的差异化调控机制，明确其通过介导骨重塑失衡、调控衰老相关炎症微环境及参与Wnt/β-catenin、MAPK等关键信号通路，形成跨细胞、多维度的骨代谢调控网络。同时，本文系统梳理了乳酰化相关生物标志物的研究进展与临床转化潜能，为老年性骨质疏松症的发病机制研究提供了更系统的理论支撑，为临床防治策略优化提供了创新性思路与潜在干预靶点。

英文摘要:

Senile osteoporosis is a common degenerative skeletal disease that seriously endangers the health of the elderly population. It is characterized by progressive bone loss, destruction of bone tissue microstructure and decreased bone strength. Its core hazard is a significant increase in the risk of fragility fractures, which in turn induce various complications. With the intensification of global population aging and the transformation of modern lifestyles, the incidence of this disease has been on the rise. It not only impairs the physical health and independent living ability of patients and reduces their quality of life, but also imposes a heavy disease burden and economic pressure on the healthcare system. As a novel post-translational modification that has attracted much attention in recent years, lactylation has gradually been recognized to pay key regulatory roles in multiple biological fields, such as cellular signal transduction, metabolic reprogramming and immune function regulation. In particular, it shows important potential value in maintaining bone metabolic homeostasis and regulating the functions of bone-related cells. This paper constructs a systematic regulatory framework of "lactylation-osteocyte function-bone metabolic microenvironment-signaling pathway". It integrates the differential regulatory mechanisms of lactylation on osteoblasts, osteoclasts and bone marrow mesenchymal stem cells, and clarifies that lactylation forms a cross-cellular, multi-dimensional bone metabolic regulatory network by mediating bone remodeling imbalance, regulating the aging-related inflammatory microenvironment and participating in key signaling pathways including Wnt/β-catenin and MAPK. Meanwhile, this paper systematically reviews the research progress in the discovery of lactylation-related biomarkers and their clinical transformation potential, providing a more systematic theoretical basis for the study of the pathogenesis of senile osteoporosis, as well as innovative ideas and potential intervention targets for the optimization of clinical prevention and treatment strategies.

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