ANALYSIS OF GCIP FUNCTION IN RHEUMATOID ARTHRITIS

Abstract

Rheumatoid arthritis is a condition that affects people globally, with a prevalence that varies between 0.1% to 2%, and unfortunately, current treatments are ineffective for about 30% of patients. To find new targets for treatment, the causes of RA have to be further examined. The primary objective of this research study is to examine the role of Grap2 cyclin-D interacting protein (GCIP) in the development of RA. According to recent studies, GCIP can inhibit cell proliferation, and downregulation of GCIP may contribute to fibroblast-like synoviocytes (FLS) overgrowth in RA patients. However, most research has been conducted only in vitro, and information about the mechanism of GCIP function in FLS is still limited. Based on the research findings of an in vivo mouse model, it was observed that the expression of GCIP is downregulated in mice induced with RA compared to untreated mice. Further research is needed to fully comprehend the role of GCIP in RA and its potential therapeutic implications