Wang Jinlong, Xiong Yibai, Song Zhiqi, Li Yanhong, Zhang Ling, Qin Chuan
Institute of Laboratory Animal Sciences, CAMS and Comparative Medicine Center, PUMC, Beijing, China.
Changping National Laboratory (CPNL), Beijing, China.
Animal Model Exp Med. 2025 May;8(5):829-841. doi: 10.1002/ame2.12573. Epub 2025 Mar 3.
The World Health Organization has declared that COVID-19 no longer constitutes a "public health emergency of international concern," yet the long-term impact of SARS-CoV-2 infection on bone health continues to pose new challenges for global public health. In recent years, numerous animal model and clinical studies have revealed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to secondary osteoporosis. The mechanisms involved are related to the virus's direct effects on bone tissue, dysregulation of the body's inflammatory response, hypoxia, noncoding RNA imbalance, and metabolic abnormalities. Although these studies have unveiled the connection between SARS-CoV-2 infection and osteoporosis, current research is not comprehensive and in depth. Future studies are needed to evaluate the long-term effects of SARS-CoV-2 on bone density and metabolism, elucidate the specific mechanisms of pathogenesis, and explore potential interventions. This review aims to collate existing research literature on SARS-CoV-2 infection-induced secondary osteoporosis, summarize the underlying mechanisms, and provide direction for future research.
世界卫生组织已宣布新冠不再构成“国际关注的突发公共卫生事件”，然而，严重急性呼吸综合征冠状病毒2（SARS-CoV-2）感染对骨骼健康的长期影响继续给全球公共卫生带来新挑战。近年来，众多动物模型和临床研究表明，SARS-CoV-2感染可导致继发性骨质疏松。其涉及的机制与病毒对骨组织的直接作用、机体炎症反应失调、缺氧、非编码RNA失衡及代谢异常有关。尽管这些研究揭示了SARS-CoV-2感染与骨质疏松之间的联系，但目前的研究并不全面和深入。未来需要开展研究以评估SARS-CoV-2对骨密度和代谢的长期影响，阐明具体发病机制，并探索潜在干预措施。本综述旨在整理关于SARS-CoV-2感染所致继发性骨质疏松的现有研究文献，总结潜在机制，并为未来研究提供方向。
