Cheng Ying, Lin Shangjin, Cao Ziyi, Yu Runzhi, Fan Yongqian, Chen Jie
Department of Gastroenterology, Huadong Hospital Affiliated to Fudan University, Shanghai 200040 China; Shanghai Key Laboratory of Clinical Geriatric Medicine, Shanghai 200040 China.
Department of Orthopedics, Huadong Hospital Affiliated to Fudan University, Shanghai 200040 China; Shanghai Key Laboratory of Clinical Geriatric Medicine, Shanghai 200040 China.
Int Immunopharmacol. 2025 Feb 6;147:114056. doi: 10.1016/j.intimp.2025.114056. Epub 2025 Jan 11.
With the exacerbation of global population aging, sarcopenia has become an increasingly recognized public health issue. Sarcopenia, characterized by a progressive decline in skeletal muscle mass, strength, and function, significantly impacts the quality of life in the elderly. Herein, we explore the role of chroniclow-gradeinflammation in the development of sarcopenia and its underlying molecular mechanisms, including chronic inflammation-associated signaling pathways, immunosenescence, obesity and lipid infiltration, gut microbiota dysbiosis and intestinal barrier disruption, and the decline of satellite cells. The interplay and interaction of these molecular mechanisms provide new perspectives on the complexity of the pathogenesis of sarcopenia and offer a theoretical foundation for the development of future therapeutic strategies.
随着全球人口老龄化的加剧，肌肉减少症已成为一个日益受到认可的公共卫生问题。肌肉减少症的特征是骨骼肌质量、力量和功能逐渐下降，对老年人的生活质量有显著影响。在此，我们探讨慢性低度炎症在肌肉减少症发生发展中的作用及其潜在分子机制，包括慢性炎症相关信号通路、免疫衰老、肥胖和脂质浸润、肠道微生物群失调和肠屏障破坏以及卫星细胞的减少。这些分子机制之间的相互作用为肌肉减少症发病机制的复杂性提供了新的视角，并为未来治疗策略的开发提供了理论基础。
