Division of Bone and Mineral Diseases, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8301, St. Louis, MO, 63110, USA.
Semin Immunopathol. 2019 Sep;41(5):607-618. doi: 10.1007/s00281-019-00753-4. Epub 2019 Sep 13.
The inflammasomes are intracellular protein complexes that are assembled in response to a variety of perturbations including infections and injuries. Failure of the inflammasomes to rapidly clear the insults or restore tissue homeostasis can result in chronic inflammation. Recurring inflammation is also provoked by mutations that cause the constitutive assembly of the components of these protein platforms. Evidence suggests that chronic inflammation is a shared mechanism in bone loss associated with aging, dysregulated metabolism, autoinflammatory, and autoimmune diseases. Mechanistically, inflammatory mediators promote bone resorption while suppressing bone formation, an imbalance which over time leads to bone loss and increased fracture risk. Thus, while acute inflammation is important for the maintenance of bone integrity, its chronic state damages this tissue. In this review, we discuss the role of the inflammasomes in inflammation-induced osteolysis.
炎症小体是细胞内的蛋白质复合物,在受到感染和损伤等多种刺激时会组装。如果炎症小体不能迅速清除这些刺激物或恢复组织内稳态,就会导致慢性炎症。突变也会引发反复的炎症,导致这些蛋白质平台的组成成分持续组装。有证据表明,慢性炎症是与衰老、代谢失调、自身炎症和自身免疫性疾病相关的骨丢失的共同机制。从机制上讲,炎症介质促进骨质吸收,同时抑制骨质形成,这种不平衡随着时间的推移会导致骨质流失和骨折风险增加。因此,虽然急性炎症对维持骨骼完整性很重要,但慢性炎症会损害这种组织。在这篇综述中,我们讨论了炎症小体在炎症诱导的溶骨性骨丢失中的作用。