Activation and Function of NLRP3 Inflammasome in Bone and Joint-Related Diseases

International Journal of Molecular Sciences

Yuri Nakaminami¹  Kenji Hata¹  Tomohiko Murakami¹  Riko Nishimura¹  Yoshifumi Takahata¹ 

[1] Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka 565-0871, Japan;

关键词: interleukin-1;    inflammasome;    NLRP3;    caspase-1;    rheumatoid arthritis;    osteoarthritis;   

DOI  :  10.3390/ijms23105365

来源: DOAJ

【 摘 要 】

Inflammation is a pivotal response to a variety of stimuli, and inflammatory molecules such as cytokines have central roles in the pathogenesis of various diseases, including bone and joint diseases. Proinflammatory cytokines are mainly produced by immune cells and mediate inflammatory and innate immune responses. Additionally, proinflammatory cytokines accelerate bone resorption and cartilage destruction, resulting in the destruction of bone and joint tissues. Thus, proinflammatory cytokines are involved in regulating the pathogenesis of bone and joint diseases. Interleukin (IL)-1 is a representative inflammatory cytokine that strongly promotes bone and cartilage destruction, and elucidating the regulation of IL-1 will advance our understanding of the onset and progression of bone and joint diseases. IL-1 has two isoforms, IL-1α and IL-1β. Both isoforms signal through the same IL-1 receptor type 1, but the activation mechanisms are completely different. In particular, IL-1β is tightly regulated by protein complexes termed inflammasomes. Recent research using innovative technologies has led to a series of discoveries about inflammasomes. This review highlights the current understanding of the activation and function of the NLRP3 (NOD-like receptor family, pyrin domain-containing 3) inflammasome in bone and joint diseases.

【 授权许可】

Unknown