Osteoporosis is a highly prevalent disorder characterized by the loss of bone mass and microarchitecture deterioration of bone tissue, attributed to various factors, including menopause (primary), aging (primary) and adverse effects of relevant medications (secondary). In recent decades, knowledge regarding the etiological mechanisms underpinning osteoporosis emphasizes that bone cellular homeostasis, including the maintenance of cell functions, differentiation, and the response to stress, is tightly regulated by autophagy, which is a cell survival mechanism for eliminating and recycling damaged proteins and organelles. With the important roles in the maintenance of cellular homeostasis and organ function, autophagy has emerged as a potential target for the prevention and treatment of osteoporosis. In this review, we update and discuss the pathophysiology of autophagy in normal bone cell life cycle and metabolism. Then, the alternations of autophagy in primary and secondary osteoporosis, and the accompanied pathological process are discussed. Finally, we discuss current strategies, limitations, and challenges involved in targeting relevant pathways and propose strategies by which such hurdles may be circumvented in the future for their translation into clinical validations and applications for the prevention and treatment of osteoporosis.

骨质疏松症是一种高度流行的疾病，其特征是骨量减少和骨组织的微结构恶化，这归因于各种因素，包括更年期（主要），衰老（主要）和相关药物的不良影响（次要）。近几十年来，有关支撑骨质疏松症的病因机制的知识强调，自噬严格控制骨细胞的稳态，包括维持细胞功能，分化和对压力的反应，这是一种用于消除和回收受损蛋白质的细胞存活机制。和细胞器。自噬在维持细胞稳态和器官功能中起着重要作用，已经成为预防和治疗骨质疏松症的潜在靶标。在这篇评论中 我们更新并讨论自噬在正常骨细胞生命周期和代谢中的病理生理。然后，讨论了原发性和继发性骨质疏松症中自噬的改变以及伴随的病理过程。最后，我们讨论了针对相关途径的当前策略，局限性和挑战，并提出了可以在将来克服这些障碍的策略，以将其转化为预防和治疗骨质疏松症的临床验证和应用。