Journal of rheumatic diseases · 2025
Genetic and epigenetic insights into systemic lupus erythematosus: linking long non-coding RNA growth arrest-specific transcript 5 and interferon signature.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Maghraby Gehad Gamal, El-Menyawi Manal Abdel-Moneim, Rehiem Hanan A Abdel, Shaker Olfat Gamil, Habib Mina M, Elgohary Rasmia
Аннотация
OBJECTIVE: Interferon (IFN) signaling, and excessive apoptosis have a well-established role in systemic lupus erythematosus (SLE) pathogenesis. Long non-coding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) has been linked to excessive apoptosis and upregulation of IFN genes. We aimed to investigate the expression of IFN-stimulated genes in SLE patients compared to healthy controls, and to assess their association with lncRNA GAS5 and clinical characteristics of SLE.
METHODS: The study included 30 SLE patients and 20 controls. IFN-stimulatory genes (interferon-induced protein 44-like [IFI44L] gene, MX dynamin like GTPase 1 [MX1], IFN-induced protein with tetratricopeptide repeats 1 [IFIT1]) and GAS5 expression levels in plasma were estimated by quantitative real-time polymerase chain reaction. IFN signature score was calculated.
RESULTS: IFIT1 gene expression and IFN signature score were significantly higher in SLE patients compared to controls (p<0.001, p<0.001, respectively). LncRNA GAS5 positively correlated with IFIT1 expression (p<0.001) and IFN signature score (p=0.005). No significant associations were found between IFN gene expression or IFN signature score and disease activity (Systemic Lupus Erythematosus Disease Activity Index 2000, SLEDAI-2K) or organ damage (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index, SDI). IFI44L expression was significantly higher in SLE patients with secondary antiphospholipid syndrome (p=0.040).
CONCLUSION: IFN signature is a potential biomarker for SLE diagnosis, but it can't be relied on for the assessment of activity or damage. The correlation between lncRNA GAS5 and IFN-related gene expression suggests a possible role for GAS5 in the IFN pathway in SLE.
METHODS: The study included 30 SLE patients and 20 controls. IFN-stimulatory genes (interferon-induced protein 44-like [IFI44L] gene, MX dynamin like GTPase 1 [MX1], IFN-induced protein with tetratricopeptide repeats 1 [IFIT1]) and GAS5 expression levels in plasma were estimated by quantitative real-time polymerase chain reaction. IFN signature score was calculated.
RESULTS: IFIT1 gene expression and IFN signature score were significantly higher in SLE patients compared to controls (p<0.001, p<0.001, respectively). LncRNA GAS5 positively correlated with IFIT1 expression (p<0.001) and IFN signature score (p=0.005). No significant associations were found between IFN gene expression or IFN signature score and disease activity (Systemic Lupus Erythematosus Disease Activity Index 2000, SLEDAI-2K) or organ damage (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index, SDI). IFI44L expression was significantly higher in SLE patients with secondary antiphospholipid syndrome (p=0.040).
CONCLUSION: IFN signature is a potential biomarker for SLE diagnosis, but it can't be relied on for the assessment of activity or damage. The correlation between lncRNA GAS5 and IFN-related gene expression suggests a possible role for GAS5 in the IFN pathway in SLE.