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Existing studies have shown that PC-1 plays a pivotal role in bone remodeling and that PC-1 deficiency results in disrupted bone remodeling, which markedly affects bone mass and skeletal development. This review describes the molecular structure and biological function of PC-1 and analyzes the mechanism by which it maintains bone homeostasis and regulates osteoblast and osteoclast activity. Particular emphasis is placed on the role of PC-1 in mechanical force-triggered bone remodeling and its interaction with the transcriptional co-activator tafazzin. 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