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<p><?tk 3?>Rheumatoid arthritis (RA), a chronic autoimmune condition that causes joint inflammation due to altered genetic expression in synovial tissue, affects 1% of the world’s population. miRNAs play a crucial role in regulating telomere length and gene expression. Elevated miR-155 expression significantly promotes RA progression by inhibiting SOCS1, an anti-inflammatory gene, and thereby enhancing the production of IL-1 and TNF-α. miR-155 has also been found to target the shelterin complex, resulting in shorter telomeres. The current study was designed to understand the molecular mechanism underlying the miR-155-SOCS1-TL axis in RA. We observed shorter telomere lengths, reduced SOCS1, and elevated miR-155 expression in RA patients relative to the control. The results of the Pearson correlation coefficient confirmed the negative correlation of miR-155 with the SOCS1 gene and telomere length. The results of univariate and multivariate logistic regression analyses did not indicate any association between genetic parameters and age or sex. The promoter analysis of the SOCS1 gene revealed the presence of G-rich sequences and a CCAATT box. Docking of miR-155 with SOCS1 promoter 1 (− 501 to + 10&#xa0;bp) and 2 (− 1000 to − 500&#xa0;bp) revealed binding scores of − 993.30 and − 851.57&#xa0;kcal/mol. Similarly, the molecular interaction analysis of miR-155 with TRF1 yielded a docking score of − 324.26&#xa0;kcal/mol and was further confirmed by molecular simulations and MM-PBSA free-energy calculations. Together, the study findings suggested that the miR-155-SOCS1-TL axis could be a promising therapeutic target for RA management.</p>

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miR-155-SOCS1-Telomere Length Axis: A Tripartite and Multifaceted Approach To Understanding Rheumatoid Arthritis Pathophysiology

  • 期刊论文

  • 发表日期：

    2026年1月19日

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  • Shanza Tariq,
  • Saima Ejaz,
  • Ayesha Liaqat,
  • Sahar Sarwar,
  • Fatma Hussain,
  • Muafia Begum,
  • Farzana Zafar,
  • Zamir Hussain,
  • Saadiya Zia

摘要

Rheumatoid arthritis (RA), a chronic autoimmune condition that causes joint inflammation due to altered genetic expression in synovial tissue, affects 1% of the world’s population. miRNAs play a crucial role in regulating telomere length and gene expression. Elevated miR-155 expression significantly promotes RA progression by inhibiting SOCS1, an anti-inflammatory gene, and thereby enhancing the production of IL-1 and TNF-α. miR-155 has also been found to target the shelterin complex, resulting in shorter telomeres. The current study was designed to understand the molecular mechanism underlying the miR-155-SOCS1-TL axis in RA. We observed shorter telomere lengths, reduced SOCS1, and elevated miR-155 expression in RA patients relative to the control. The results of the Pearson correlation coefficient confirmed the negative correlation of miR-155 with the SOCS1 gene and telomere length. The results of univariate and multivariate logistic regression analyses did not indicate any association between genetic parameters and age or sex. The promoter analysis of the SOCS1 gene revealed the presence of G-rich sequences and a CCAATT box. Docking of miR-155 with SOCS1 promoter 1 (− 501 to + 10 bp) and 2 (− 1000 to − 500 bp) revealed binding scores of − 993.30 and − 851.57 kcal/mol. Similarly, the molecular interaction analysis of miR-155 with TRF1 yielded a docking score of − 324.26 kcal/mol and was further confirmed by molecular simulations and MM-PBSA free-energy calculations. Together, the study findings suggested that the miR-155-SOCS1-TL axis could be a promising therapeutic target for RA management.