Background: Hox Transcript Antisense Intergenic RNA (HOTAIR), a well-studied Long Non-Coding RNA (lncRNA), is known to regulate gene expression through epigenetic mechanisms, primarily by interacting with Polycomb Repressive Complex 2 (PRC2) to modify histone methylation patterns. HOTAIR can modulate the expression of inflammatory cytokines, such as TNF-α and IL-6, directly exacerbating the inflammatory environment within the joint. Its effects on synovial fibroblasts, crucial cells in rheumatoid arthritis (RA) induced joint damage, are also being investigated. HOTAIR may influence fibroblast proliferation and the production of matrix metalloproteinases (MMPs), contributing to cartilage and bone erosion. The precise mechanisms through which HOTAIR exerts its effects in RA remain an area of active research. However, the consistent observation of its dysregulation in RA patients, coupled with its established roles in epigenetic modification and immune cell regulation, strongly suggests its potential as a therapeutic target and biomarker for RA. Future research focusing on specific HOTAIR-mediated pathways could lead to the development of novel therapeutic interventions to combat this debilitating disease. We aimed to present a summary of Role of Long Non-Coding RNA (Hox Transcript Antisense Intergenic RNA) in Rheumatoid Arthritis Patients.

Conclusion: HOTAIR's involvement in RA pathogenesis is multifaceted and involves interactions with numerous molecules and pathways. Further research is needed to clarify its precise mechanisms of action and the specific genes it regulates in RA, as well as exploring the complex interplay with other non-coding RNAs and signaling cascades.