Muscle-bone biochemical crosstalk in osteosarcopenia: focusing on mechanisms and potential therapeutic strategies.

IF 3.9 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Journal of Endocrinology Pub Date : 2025-09-16 Print Date: 2025-09-01 DOI:10.1530/JOE-25-0234
Qinzuo Dong, Danyang Li, Ke Zhang, Hua Shi, Ming Cai, Yangdi Li, Rong Zhao, Dongdong Qin
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引用次数: 0

Abstract

Osteosarcopenia (OS) is a syndrome defined by the concurrent presence of sarcopenia and osteoporosis in the elderly population, which markedly elevates the risk of falls, fractures, and mortality. Recent studies demonstrate that disruption of muscle-bone biochemical crosstalk emerges as a key driver of OS pathogenesis, and that targeting pivotal mediators and pathways can concurrently restore musculoskeletal homeostasis. However, the precise molecular mechanisms and targeted therapeutic strategies remain inadequately explored. This review systematically summarizes the epidemiological risk factors and pathophysiological mechanisms underpinning OS, with emphasis on the interplay within musculoskeletal metabolism among myokines (e.g., fibroblast growth factors 21, FGF21, and irisin), osteokines (e.g., osteocalcin, OCN, receptor activator of nuclear factor-κB ligand, RANKL, and sclerostin, SOST), adipokines, and shared signaling pathways such as mitochondria-associated axes, Wnt/β-catenin, and nuclear factor-κB (NF-κB), as well as discusses the potential efficacy of direct and indirect interventions targeting these factors and biochemical signals, which provides innovative strategies and prospective research directions for developing precision-targeted therapies against OS and other degenerative musculoskeletal disorders. In addition, we propose that precise modulation of muscle-bone signaling constitutes a promising approach to treat OS. Future efforts should prioritize standardizing diagnostic criteria and advancing the development of therapies targeting critical muscle-bone biochemical interaction nodes to optimize the management of musculoskeletal comorbidities in the aging population.

骨骼肌减少症中的肌肉-骨生化串扰:关注机制和潜在的治疗策略。
骨骼肌减少症(OS)是老年人群中骨骼肌减少症和骨质疏松症同时存在的一种综合征,它显著增加了跌倒、骨折和死亡的风险。最近的研究表明,骨骼肌生化串扰的破坏是骨性骨肉瘤发病的一个关键驱动因素,并且靶向关键介质和途径可以同时恢复肌肉骨骼稳态。然而,精确的分子机制和靶向治疗策略仍未充分探索。本文系统总结了OS的流行病学危险因素和病理生理机制,重点介绍了肌肉骨骼代谢中肌因子(如成纤维细胞生长因子21、FGF21和鸢尾素)、骨因子(如骨钙素、OCN、核因子-κB配体受体激活因子RANKL和硬化蛋白SOST)、脂肪因子以及线粒体相关轴、Wnt/β-catenin和核因子κB (NF-κB)等共享信号通路的相互作用。并探讨了针对这些因素和生化信号的直接和间接干预的潜在疗效,为开发针对骨肉瘤和其他退行性肌肉骨骼疾病的精准靶向治疗提供了创新策略和前瞻性研究方向。此外,我们提出,精确调节肌肉-骨骼信号是治疗骨肉瘤的一种很有前景的方法,未来的努力应优先考虑标准化诊断标准,并推进针对关键肌肉-骨骼生化相互作用节点的治疗方法的开发,以优化老年人群中肌肉-骨骼合并症的管理。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Endocrinology
Journal of Endocrinology 医学-内分泌学与代谢
CiteScore
7.90
自引率
2.50%
发文量
113
审稿时长
4-8 weeks
期刊介绍: Journal of Endocrinology is a leading global journal that publishes original research articles, reviews and science guidelines. Its focus is on endocrine physiology and metabolism, including hormone secretion; hormone action; biological effects. The journal publishes basic and translational studies at the organ, tissue and whole organism level.
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