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As a kind of organelle, mitochondria are the main places for aerobic respiration and ATP production, and their structure and function are essential for cell life. The imbalance of mitochondrial structure and function can lead to a series of diseases, such as degenerative diseases, myasthenia gravis, osteoporosis, etc. There is a close relationship between mitochondria and osteoporosis, and it can participate in bone metabolism in many ways. Among them, the specific regulatory mechanisms mainly focus on the energy supply pathway of oxidative phosphorylation, the production and clearance of reactive oxygen species (ROS), mitochondrial dynamics, and so on. Regulating the structure and function of mitochondria is a potential way to treat osteoporosis. Therefore, this paper reviews the recent research and latest progress of mitochondria and osteoporosis, in order to further clarify the relationship and mechanism between them, and provide new ideas for the treatment of osteoporosis [ABSTRACT FROM AUTHOR]

The endoplasmic reticulum (ER) is an important membranous organelle responsible for protein synthesis, folding and processing, lipid synthesis, and Ca2+balance. Under the influence of some factors, the structure and function of ER are disturbed, leading to ER stress. Under ER stress, ER maintains its normal structure and function mainly through the processes of unfolded protein reaction and ER autophagy. There is a close relationship between ER stress and many diseases, such as cancer, inflammatory diseases, neurodegenerative diseases, osteoporosis, and so on. Under ER stress, the unfolded protein response and ER autophagy may participate in the regulation of bone metabolism, which may be a potential target for the treatment of osteoporosis. Therefore, we review the existing relevant literature and the latest research reports, aiming to elucidate the influence and mechanism of the unfolded protein response and ER autophagy on osteoporosis, and to provide new ideas for further clarifying the pathogenesis and treatment of osteoporosis. [ABSTRACT FROM AUTHOR]

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Copyright of Chinese Journal of Osteoporosis is the property of Chinese Journal of Osteoporosis and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)