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Current Rheumatology Reviews

Editor-in-Chief

ISSN (Print): 1573-3971
ISSN (Online): 1875-6360

Research Article

Serum Levels of Long Non-coding RNAs NEAT1, GAS5, and GAPLINC Altered in Rheumatoid Arthritis

Author(s): Roghayeh Tofigh, Mohammadali Hosseinpourfeizi*, Reza Safaralizadeh, Sepideh Ghoddusifar and Behzad Baradaran*

Volume 20, Issue 2, 2024

Published on: 06 October, 2023

Page: [182 - 190] Pages: 9

DOI: 10.2174/0115733971251184230921042511

Price: $65

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Abstract

Background: Rheumatoid arthritis (RA), an autoimmune joint inflammatory disease, presents a significant challenge due to its prevalence, particularly among women, affecting around 6% of individuals over the age of 65. Novel insights into disease mechanisms are crucial for improved diagnostic and therapeutic approaches.

Objective: Long non-coding RNAs (lncRNAs) have emerged as potential contributors to the pathogenesis of various autoimmune diseases, including RA. This study aims to investigate the unique roles of four lncRNAs-NEAT1, GAS5, TMEVPG1, and GAPLINC-in the etiology of RA.

Methods: Leveraging isolated serum samples from RA patients and healthy controls, we comprehensively evaluated the expression profiles of these lncRNAs.

Results: Notably, our findings unveil a distinctive landscape of lncRNA expressions in RA. Among them, GAPLINC exhibited a significantly elevated average expression in the serum samples of RA patients, suggesting a potential biomarker candidate for disease stratification. Importantly, reduced expression of NEAT1 and GAS5 was observed in RA patients, highlighting their possible roles as diagnostic and prognostic markers. Conversely, TMEVPG1 displayed unaltered expression levels in RA samples.

Conclusion: Our study introduces a novel dimension to RA research by identifying NEAT1, GAS5, and GAPLINC as promising serological biomarkers. These findings hold significant clinical implications, offering potential avenues for improved diagnosis, disease monitoring, and therapeutic interventions in RA.

Graphical Abstract

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