LncRNA HOXA‐AS2 Can Predict the Risk of Acute Respiratory Distress Syndrome and 28‐Day Mortality in Patients With Sepsis
ABSTRACT Objective This study aimed to explore the diagnostic and predictive value of lncRNA HOXA‐AS2 for acute respiratory distress syndrome (ARDS) and 28‐day mortality in sepsis patients. Methods The levels of HOXA‐AS2 in sepsis and ARDS patients were detected by real‐time quantitative reverse tra...
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| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2025-05-01
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| Series: | The Clinical Respiratory Journal |
| Subjects: | |
| Online Access: | https://doi.org/10.1111/crj.70082 |
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| Summary: | ABSTRACT Objective This study aimed to explore the diagnostic and predictive value of lncRNA HOXA‐AS2 for acute respiratory distress syndrome (ARDS) and 28‐day mortality in sepsis patients. Methods The levels of HOXA‐AS2 in sepsis and ARDS patients were detected by real‐time quantitative reverse transcription PCR (RT‐qPCR). The receiver operating curve (ROC) curve was used to evaluate the diagnostic value of HOXA‐AS2 for sepsis and ARDS. The K‐M curve was used to evaluate the effect of HOXA‐AS2 on the prognosis. Logistic regression analysis and COX regression analysis were used to explore the risk factors influencing ARDS and death. Additionally, an ARDS cell model was constructed to explore the effects of HOXA‐AS2 on cell viability, inflammation, and endothelial glycocalyx. Results HOXA‐AS2 decreased in sepsis patients who developed ARDS and died. This molecule can not only serve as a diagnostic marker for sepsis but also act as a risk factor to predict the risk of ARDS and death within 28 days in patients with sepsis. Sepsis patients with low levels of HOXA‐AS2 are more prone to ARDS and death. In cells attacked by lipopolysaccharide (LPS), overexpression of HOXA‐AS2 inhibited apoptosis, inflammation, and the degradation of endothelial glycocalyx. Conclusion In sepsis patients, HOXA‐AS2 has the potential to serve as a predictive marker for ARDS and 28‐day mortality. This molecule may delay the progression of ARDS by inhibiting inflammation and the degradation of the endothelial glycocalyx. |
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| ISSN: | 1752-6981 1752-699X |