[The role of NLRP3 inflammasome in the pathogenesis of ankylosing spondylitis research progress].

Abstract

Ankylosing Spondylitis(AS) is a chronic inflammatory disease primarily affecting the spine and sacroiliac joints, with a higher prevalence in young males. Without timely diagnosis and treatment, it can progress to spinal ankylosis, joint function loss, and disability. The exact pathogenesis remains incompletely understood, leaving some patients unresponsive to current treatments and facing poor outcomes. In recent years, the role of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in the pathogenesis of AS has attracted much attention. Upon activation, the NLRP3 inflammasome promotes the activation of cysteine protease 1 (caspase-1), which subsequently cleaves pro-interleukin 1β (pro-IL-1β) into its active form, IL-1β, to aggravate inflammatory responses and bone destruction. This review summarizes the regulatory mechanism of NLRP3 inflammasome in AS and discusses its therapeutic potential. The aim is to provide a rationale for exploring the underlying pathogenesis of AS and for developing novel targeted therapies.