Cell life-or-death events in osteoporosis: All roads lead to mitochondrial dynamics

线粒体 骨重建 信号转导 程序性细胞死亡 细胞代谢 骨质疏松症 细胞 细胞生物学 生物 细胞凋亡 内分泌学 生物化学
作者
Zhichao Li,Songlin Liang,Liqing Ke,Mengjie Wang,Kuanhui Gao,Dandan Li,Zhanwang Xu,Nianhu Li,Peng Zhang,Wenxiang Cheng
出处
期刊:Pharmacological Research [Elsevier BV]
卷期号:208: 107383-107383 被引量:2
标识
DOI:10.1016/j.phrs.2024.107383
摘要

Mitochondria exhibit heterogeneous shapes and networks within and among cell types and tissues, also in normal or osteoporotic bone tissues with complex cell types. This dynamic characteristic is determined by the high plasticity provided by mitochondrial dynamics and is stemmed from responding to the survival and functional requirements of various bone cells in a specific microenvironments. In contrast, mitochondrial dysfunction, induced by dysregulation of mitochondrial dynamics, may act as a trigger of cell death signals, including common apoptosis and other forms of programmed cell death (PCD). These PCD processes consisting of tightly structured cascade gene expression events, can further influence the bone remodeling by facilitating the death of various bone cells. Mitochondrial dynamics, therefore, drive the bone cells to stand at the crossroads of life and death by integrating external signals and altering metabolism, shape, and signal-response properties of mitochondria. This implies that targeting mitochondrial dynamics displays significant potential in treatment of osteoporosis. Considerable effort has been made in osteoporosis to emphasize the parallel roles of mitochondria in regulating energy metabolism, calcium signal transduction, oxidative stress, inflammation, and cell death. However, the emerging field of mitochondrial dynamics-related PCD is not well understood. Herein, to bridge the gap, we outline the latest knowledge on mitochondrial dynamics regulating bone cell life or death during normal bone remodeling and osteoporosis.
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