Suppr超能文献

PI3K/Akt/mTOR信号通路在骨质疏松症中的作用及机制研究

Research on the role and mechanism of the PI3K/Akt/mTOR signalling pathway in osteoporosis.

作者信息

Liu Chuanlong, Zhang Jianqiang, Ye Ziyu, Luo Ji, Peng Bing, Wang Zhexiang

机构信息

Hunan Hospital of Integrated Traditional Chinese and Western Medicine, Changsha, Hunan, China.

Hunan University of Chinese Medicine, Changsha, Hunan, China.

出版信息

Front Endocrinol (Lausanne). 2025 May 12;16:1541714. doi: 10.3389/fendo.2025.1541714. eCollection 2025.

Abstract

Osteoporosis is a systemic metabolic bone disease characterised mainly by reduced bone mass, bone microstructure degradation, and loss of bone mechanical properties. As the world population ages, more than 200 million people worldwide suffer from the pain caused by osteoporosis every year, which severely affects their quality of life. Moreover, the prevalence of osteoporosis continues to increase. The pathogenesis of osteoporosis is highly complex and is closely related to apoptosis, autophagy, oxidative stress, the inflammatory response, and ferroptosis. The PI3K/Akt/mTOR signalling pathway is one of the most crucial intracellular signal transduction pathways. This pathway is not only involved in bone metabolism and bone remodelling but also closely related to the proliferation and differentiation of osteoblasts, osteoclasts, and bone marrow mesenchymal stem cells. Abnormal activation or inhibition of the PI3K/Akt/mTOR signalling pathway can disrupt the balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption, ultimately leading to the development of osteoporosis. This review summarises the molecular mechanisms by which the PI3K/Akt/mTOR signalling pathway mediates five pathological mechanisms, namely, apoptosis, autophagy, oxidative stress, the inflammatory response, and ferroptosis, in the regulation of osteoporosis, aiming to provide a theoretical basis for the development of novel and effective therapeutic drugs and intervention measures for osteoporosis prevention and treatment.

摘要

骨质疏松症是一种全身性代谢性骨病,主要特征为骨量减少、骨微结构破坏以及骨力学性能丧失。随着世界人口老龄化,全球每年有超过2亿人遭受骨质疏松症引起的疼痛,这严重影响了他们的生活质量。此外,骨质疏松症的患病率持续上升。骨质疏松症的发病机制高度复杂,与细胞凋亡、自噬、氧化应激、炎症反应和铁死亡密切相关。PI3K/Akt/mTOR信号通路是细胞内最关键的信号转导通路之一。该通路不仅参与骨代谢和骨重塑,还与成骨细胞、破骨细胞和骨髓间充质干细胞的增殖和分化密切相关。PI3K/Akt/mTOR信号通路的异常激活或抑制会破坏成骨细胞介导的骨形成与破骨细胞介导的骨吸收之间的平衡,最终导致骨质疏松症的发生。本综述总结了PI3K/Akt/mTOR信号通路介导细胞凋亡、自噬、氧化应激、炎症反应和铁死亡这五种病理机制在骨质疏松症调控中的分子机制,旨在为开发新型有效的治疗药物以及骨质疏松症防治的干预措施提供理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d28/12104071/eda10ec20c84/fendo-16-1541714-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验