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炎症因子在绝经后T2DM骨代谢中的作用与分子机制的研究进展
Research Progress on the Role of Inflammatory Cytokines and Molecular Mechanisms in Bone Metabolism in Postmenopausal T2DM

DOI: 10.12677/jcpm.2025.42163, PP. 193-201

Keywords: 炎症因子,T2DM,骨代谢,绝经后女性,分子机制,精准治疗
Inflammatory Cytokines
, T2DM, Bone Metabolism, Postmenopausal Women, Molecular Mechanisms, Precision Treatment

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Abstract:

T2DM与骨代谢失衡之间的关系引起了广泛关注,尤其是在绝经后女性中,骨质疏松和骨折风险显著增加。多项研究已表明,炎症因子在T2DM患者骨代谢失衡中发挥着核心作用。炎症因子(如TNF-α、IL-1β、IL-6等)通过增强破骨细胞活性和抑制成骨细胞功能,导致骨吸收和骨生成失衡,加剧骨质丧失。此外,慢性低度炎症、胰岛素抵抗和高血糖状态共同作用,进一步扰乱骨代谢平衡。本文综述了炎症因子在T2DM骨代谢中的作用机制,重点分析了炎症因子通过Wnt/β-Catenin、RANK/RANKL/OPG、PI3K/Akt以及MAPK等信号通路在骨代谢调控中的作用。特别是在绝经后女性群体中,随着雌激素水平下降和脂肪代谢改变,炎症因子的作用显著增强,从而加剧骨代谢失衡。通过探讨这些分子机制,以期为临床个性化治疗提供理论依据,进而有效降低骨折风险,推动精准治疗策略的实施。
The relationship between T2DM and bone metabolism imbalance has garnered considerable attention, particularly in postmenopausal women, in whom the risk of osteoporosis and fractures is significantly elevated. Numerous studies have shown that inflammatory cytokines play a pivotal role in the bone metabolic imbalance observed in T2DM patients. Inflammatory cytokines (such as TNF-α, IL-1β, IL-6, etc.) enhance osteoclast activity and inhibit osteoblast function, thereby leading to an imbalance between bone resorption and formation and accelerating bone loss. Furthermore, chronic low-grade inflammation, insulin resistance, and hyperglycemia collectively disrupt bone metabolism. This review summarizes the mechanisms through which inflammatory cytokines affect bone metabolism in T2DM, with a focus on their roles in bone metabolism regulation via signaling pathways such as Wnt/β-Catenin, RANK/RANKL/OPG, PI3K/Akt, and MAPK. Particularly in postmenopausal women, the decline in estrogen levels and changes in lipid metabolism significantly amplify the effects of inflammatory cytokines, thereby exacerbating the imbalance in bone metabolism. By exploring these molecular mechanisms, we aim to provide a theoretical foundation for clinical personalized treatments, thereby effectively reducing fracture risk and promoting the implementation of precision therapeutic strategies.

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