학술논문

Dysregulation of long non-coding RNAs in Takayasu arteritis: A proof-of-concept study
Document Type
Review Paper
Source
Clinical Rheumatology: Journal of the International League of Associations for Rheumatology. 43(3):1253-1259
Subject
Biomarkers
HIF1A-AS1
HOTAIR
Long non-coding RNA
Takayasu arteritis
THRIL
Language
English
ISSN
0770-3198
1434-9949
Abstract
Takayasu arteritis (TAK) is a rare systemic vasculitis primarily affecting the aorta and its major branches. Early diagnosis is critical to prevent severe vascular complications, yet current biomarkers are insufficient. This proof-of-concept study explores the potential of long non-coding RNAs (lncRNAs) in TAK, an area largely unexplored. In this cross-sectional study, 53 TAK patients, 53 healthy controls, and 10 rheumatoid arthritis (RA) patients were enrolled. Clinical evaluations, disease activity assessments, and lncRNA expression levels were analyzed. TAK patients exhibited significant dysregulation in several lncRNAs, including THRIL (19.4, 11.1–48.8 vs. 62.5, 48.6–91.4 arbitrary units [a.u.]; p < 0.0001), HIF1A-AS1 (4.5, 1.8–16.6 vs. 26.5, 19.8–33.7 a.u.; p < 0.0001), MALAT-1 (26.9, 13.8–52.5 vs. 92.1, 58.5–92.1 a.u.; p < 0.0001), and HOTAIR (8.0, 2.5–24.5 vs. 36.0, 30.0–43.8 a.u.; p < 0.0001), compared to healthy controls. Notably, HOTAIR (area under the ROC curve [AUC] = 0.825), HIF1A-AS1 (AUC = 0.820), and THRIL (AUC = 0.781) demonstrated high diagnostic potential with superior specificity (approximately 95%). While lncRNAs showed diagnostic promise, no significant correlations with TAK activity were observed. Comparative analysis with RA patients revealed distinct lncRNA expression patterns. This study unveils significant dysregulation of lncRNAs THRIL, HIF1A-AS1, and HOTAIR in TAK patients, underscoring their potential as biomarkers and opening avenues for further research into the mechanistic roles of these lncRNAs in TAK pathogenesis.