The double-edged sword of lncRNAs in rheumatoid arthritis: from controlling the disease to its progress.

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by chronic inflammatory responses in the joints, synovial hyperplasia, persistent abnormal proliferation of fibroblast-like synoviocytes (FLSs), and cartilage erosion, leading to joint swelling and destruction. The underlying mechanisms of this disease entail a complex interplay of factors, with long noncoding RNAs (lncRNAs) serving as the main contributors. These lncRNAs, which are over 200 bp in length, are involved in regulating inflammatory responses, joint damage, and FLS growth. Studies have shown that lncRNAs have a dual function in the progression of RA, as they can both promote the disease and control inflammatory responses to reduce symptoms. Nevertheless, our current understanding of the dual function of lncRNAs in the development of RA is incomplete, and the exact molecular mechanisms involved in this process remain unclear. This study aims to elucidate the molecular mechanisms by which lncRNAs exert their inhibitory and stimulatory effects, as well as explore the potential of lncRNAs in diagnosing, predicting the prognosis, and targeting therapy for RA.