Abstract

A BRIEF REVIEW OF PYROPTOSIS BY NLRP3/CASPASE- 1/GASDERMIN D IN RHEUMATOID ARTHRITIS

Abdul Hafeel M. P.* and Bijesh Vatakkeel and Najma K.

Abstract

Rheumatoid arthritis, a persistent autoimmune condition, results in inflammation that extends beyond the joints, causing damage to other organs in the body. Compared to men, women experience this twice or three times faster, with the disease affecting 1–2% of the global population. All of this joint degradation leads to deformities and bone degradation, which is the progressive disintegration or deterioration of bone structure, which often results in painful symptoms for the patient. RA commonly manifests as weight loss, fatigue, fever, rheumatoid nodules beneath the skin, and morning stiffness of the affected joints persisting for more than thirty minutes. This illness frequently shows symptoms in people aged 35 to 60. The pathogenesis of the disease involves many different pathways. This review is mainly focused on recently explored pathways such as pyroptosis of NLRP3/caspase- 1/gasdermin-D, which results in inflammation in joints. Recent research indicates that RA may be aggravated by pyroptosis, a kind of regulated cell death that was just discovered. Interleukins such as IL-1β and IL-18 are two cytokines that are triggered during pyroptosis by NLRP3 inflammasome, which also activates caspase 1. Gasdermin D (GSDMD) can be split by caspase 1 and other caspases, and the GSDMD-N terminal opens pores in the plasma membrane that allow substances like lactate dehydrogenase (LDH) to flow out. The different immunohistochemistry methods support the increased activity of NLRP3/caspase-1/gasdermin D within the synovial fluid of RA patients.

Keywords: Rheumatoid arthritis, pyroptosis, NLRP3/caspase-1/Gasdermin-D, inflammation.