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Targeting APJ drives BNIP3-PINK1-PARKIN induced mitophagy and improves systemic inflammatory bone loss
Journal of Advanced Research ( IF 11.4 ) Pub Date : 2024-12-25 , DOI: 10.1016/j.jare.2024.12.033
Wentao Wang, Qing Wang, Wenming Li, Hao Xu, Xiaolong Liang, Wei Wang, Ning Li, Huilin Yang, Yaozeng Xu, Jiaxiang Bai, Shuli Yang, Dechun Geng

Inflammatory diseases, such as diabetes mellitus, rheumatoid arthritis, and inflammatory bowel disease, lead to systemic immune microenvironment disturbances, contributing to bone loss, yet the mechanisms by which specific receptors regulate this process in inflammatory bone loss remain poorly understood. As a G-protein-coupled receptor, the Apelin receptor plays a crucial role in the regulation of inflammation and immune microenvironment. However, the precise mechanisms governing its role in inflammatory bone loss remain incompletely understood.

中文翻译:


靶向 APJ 驱动 BNIP3-PINK1-PARKIN 诱导的线粒体自噬并改善全身炎症性骨丢失



炎症性疾病,如糖尿病、类风湿性关节炎和炎症性肠病,导致全身免疫微环境紊乱,导致骨质流失,但特异性受体在炎症性骨质流失中调节这一过程的机制仍然知之甚少。作为一种 G 蛋白偶联受体,Apelin 受体在炎症和免疫微环境的调节中起着至关重要的作用。然而,控制其在炎症性骨质流失中作用的确切机制仍不完全清楚。
更新日期:2024-12-25
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