基于骨肉疏薄理论探讨Wnt/β-catenin 信号通路在肌少-骨质疏松症共病中的生物学内涵

Exploration of Biological Implications of Wnt/β-catenin Signaling Pathway in Sarcopenia- Osteoporosis Comorbidity Based on Theory of Bone-Muscle Attenuation

摘要:

肌少-骨质疏松症（OS） 是老年人群肌肉与骨骼同步退变的常见疾病，严重影响患者的生活质量 与疾病预后。本文基于中医学“骨肉疏薄”理论，提出OS为脾肾亏虚所致的“骨枯肉薄”病机假说。在此基 础上，聚焦Wnt/β-catenin信号通路，系统阐释其在OS中的生物学内涵：在骨骼中，该通路受抑导致成骨分化 障碍，对应“肾不生髓”；在肌肉中，该通路异常活化促进纤维化，对应“脾不散精”；在肌骨对话中，其双向 调控失衡加剧共病进程，映射“骨肉不相亲”的病理状态。Wnt/β-catenin通路可视为“骨肉疏薄”理论的现 代生物学桥梁，其组织特异性失调正是中医病机在微观层面的生动写照。本研究为OS的“肌骨同治”策略开 辟新思路。

Abstract:

Abstract：Sarcopenia-osteoporosis （OS） is a common condition characterized by the simultaneous degeneration of muscle and bone in the elderly， significantly impacting patients' quality of life and clinical outcomes. Based on the traditional Chinese medicine theory of "bone-muscle attenuation， " this article proposes a pathogenic mechanism hypothesis that OS results from the spleen-kidney deficiency， leading to "withered bones and thin flesh." With that， this article focused on the Wnt/β-catenin signaling pathway to systematically elucidate its biological implications in OS： in bone tissue， inhibition of this pathway leads to impaired osteogenic differentiation， leading to "the kidney fails to generate marrow； "in muscle tissue， abnormal activation of this pathway promotes fibrosis， leading to "the spleen failing to disperse essence； "in terms of muscle-bone， an imbalance in its bidirectional regulation exacerbates the comorbidity process， reflecting the pathological state of "disharmony between bone and flesh." The Wnt/β-catenin pathway can be regarded as a modern biological bridge to the theory of “bone-muscle attenuation，” and its tissuespecific dysregulation vividly illustrates the pathogenesis of traditional Chinese medicine at the microscopic level. This study opens up new insights for the simultaneous treatment of muscle and bone strategy in OS.