Bone and Joint Reconstruction Research Center, Shafa Orthopedic Hospital, department of orthopedic, school of medicine, Iran University of Medical Sciences, Tehran, Iran.
Key Laboratory of Epigenetics and Oncology, the Research Center for Preclinical Medicine, Southwest Medical University, Luzhou 646000, Sichuan, China.
Biomed Pharmacother. 2024 Aug;177:116954. doi: 10.1016/j.biopha.2024.116954. Epub 2024 Jun 20.
Osteoporosis, characterized by compromised bone density and microarchitecture, represents a significant global health challenge, particularly in aging populations. This comprehensive review delves into the intricate signaling pathways implicated in the pathogenesis of osteoporosis, providing valuable insights into the pivotal role of signal transduction in maintaining bone homeostasis. The exploration encompasses cellular signaling pathways such as Wnt, Notch, JAK/STAT, NF-κB, and TGF-β, all of which play crucial roles in bone remodeling. The dysregulation of these pathways is a contributing factor to osteoporosis, necessitating a profound understanding of their complexities to unveil the molecular mechanisms underlying bone loss. The review highlights the pathological significance of disrupted signaling in osteoporosis, emphasizing how these deviations impact the functionality of osteoblasts and osteoclasts, ultimately resulting in heightened bone resorption and compromised bone formation. A nuanced analysis of the intricate crosstalk between these pathways is provided to underscore their relevance in the pathophysiology of osteoporosis. Furthermore, the study addresses some of the most crucial long non-coding RNAs (lncRNAs) associated with osteoporosis, adding an additional layer of academic depth to the exploration of immune system involvement in various types of osteoporosis. Finally, we propose that SKP1 can serve as a potential biomarker in osteoporosis.
骨质疏松症的特征是骨密度和微结构受损，是一个全球性的重大健康挑战，特别是在老龄化人口中。本综述深入探讨了与骨质疏松症发病机制相关的复杂信号通路，为信号转导在维持骨稳态中的关键作用提供了有价值的见解。该探索涵盖了细胞信号通路，如 Wnt、Notch、JAK/STAT、NF-κB 和 TGF-β，它们在骨重塑中都起着至关重要的作用。这些通路的失调是骨质疏松症的一个促成因素，需要深入了解它们的复杂性，以揭示骨丢失的分子机制。本综述强调了信号中断在骨质疏松症中的病理意义，强调了这些偏差如何影响成骨细胞和破骨细胞的功能，最终导致骨吸收增加和骨形成受损。对这些通路之间复杂的串扰进行了细致的分析，以强调它们在骨质疏松症病理生理学中的相关性。此外，该研究还探讨了一些与骨质疏松症相关的最重要的长非编码 RNA（lncRNA），为探讨免疫系统在各种类型骨质疏松症中的作用增加了学术深度。最后，我们提出 SKP1 可以作为骨质疏松症的一个潜在生物标志物。
