Department of Orthopaedics, First Affiliated Hospital of China Medical University, Shenyang, China.
Department of Burn Surgery, Changhai Hospital, the Naval Medical University, Shanghai, China.
Front Endocrinol (Lausanne). 2021 Jan 8;11:548812. doi: 10.3389/fendo.2020.548812. eCollection 2020.
Osteoporosis has become a worldwide disease characterized by a reduction in bone mineral density and the alteration of bone architecture leading to an increased risk of fragility fractures. And an increasing number of studies have indicated that osteoblasts undergo a large number of programmed death events by many different causes in osteoporosis and release NLRP3 and interleukin (e.g., inflammatory factors), which play pivotal roles in contributing to excessive differentiation of osteoclasts and result in exaggerated bone resorption. NLRP3 is activated during pyroptosis and processes the precursors of IL-1β and IL-18 into mature forms, which are released into the extracellular milieu accompanied by cell rupture. All of these compounds are the classical factors of pyroptosis. The cellular effects of pyroptosis are commonly observed in osteoporosis. Although many previous studies have focused on the pathogenesis of these inflammatory factors in osteoporosis, pyroptosis has not been previously evaluated. In this review, pyroptosis is proposed as a novel hypothesis of osteoporosis pathogenesis for the first time, thus providing a new direction for the treatment of osteoporosis in the future.
骨质疏松症已成为一种全球性疾病，其特征是骨矿物质密度降低和骨结构改变，导致脆性骨折的风险增加。越来越多的研究表明，骨质疏松症中许多不同原因可导致成骨细胞发生大量程序性死亡事件，并释放 NOD 样受体热蛋白 3（NLRP3）和白细胞介素（如炎症因子），这些在促进破骨细胞过度分化和导致骨吸收增加方面发挥关键作用。NLRP3 在细胞焦亡过程中被激活，并将 IL-1β 和 IL-18 的前体加工成熟形式，这些成熟形式伴随着细胞破裂被释放到细胞外环境中。所有这些化合物都是细胞焦亡的经典因子。细胞焦亡的细胞效应在骨质疏松症中很常见。尽管以前的许多研究都集中在这些炎症因子在骨质疏松症发病机制中的作用，但以前从未对细胞焦亡进行过评估。在这篇综述中，首次提出细胞焦亡是骨质疏松症发病机制的一个新假说，为未来骨质疏松症的治疗提供了一个新的方向。
