miR-379-5p作为生物标志物通过靶向EDN1调控脓毒症相关急性肾损伤
miR-379-5p serves as a biomarker and regulates sepsis-associated acute kidney injury via targeting EDN1.
摘要(中文译文)
脓毒症相关急性肾损伤（SA-AKI）是脓毒症患者的严重并发症，微小RNA（miRNA）参与其发生和发展。本研究探讨了miR-379-5p的临床价值及其对脂多糖（LPS）诱导的人近端肾小管上皮细胞系（HK-2）的潜在机制。研究检测了85例脓毒症患者和74例SA-AKI患者的血清miR-379-5p水平，从SA-AKI诊断、肾损伤相关性及28天生存评估等角度探讨了miR-379-5p的临床意义。构建LPS诱导的HK-2细胞模型，分析miR-379-5p对LPS诱导的HK-2细胞活力和炎症反应的调控作用，并探讨其调控机制，重点关注EDN1的参与。血清miR-379-5p低表达可区分SA-AKI与脓毒症患者，且与血清肌酐（Scr）、血尿素氮（BUN）、胱抑素C（Cys-C）、肾损伤分子-1（KIM-1）、C反应蛋白（CRP）、降钙素原（PCT）和白细胞（WBC）呈负相关。miR-379-5p低表达与28天生存率相关。LPS可抑制HK-2细胞中miR-379-5p的表达，抑制细胞活力，并促进炎症因子TNF-α、IL-1β和IL-6的浓度升高。过表达miR-379-5p可逆转LPS对HK-2细胞的作用。EDN1是miR-379-5p的直接靶基因。过表达EDN1可抵消miR-379-5p过表达对HK-2细胞的保护作用。血清miR-379-5p下调在诊断SA-AKI和预测患者28天生存方面具有潜在价值。过表达miR-379-5p通过靶向抑制EDN1保护HK-2细胞免受LPS诱导的损伤。
Abstract
Sepsis-associated acute kidney injury (SA-AKI) is a serious complication for sepsis patients, and microRNA (miRNA) is involved in its occurrence and development. This study investigated the clinical value of miR-379-5p and its potential mechanism on LPS-induced human proximal tubular epithelial cell lines (HK-2). Serum miR-379-5p levels were measured in 85 sepsis patients and 74 SA-AKI patients. The clinical significance of miR-379-5p was explored from the perspectives of SA-AKI diagnosis, kidney injury correlation, and 28-day survival assessment. The LPS-induced HK-2 cell model was constructed, and the regulatory effect of miR-379-5p on LPS-induced HK-2 cell viability and inflammatory response was analyzed. The regulatory mechanism was explored, focusing on the involvement of EDN1. Low expression of serum miR-379-5p could distinguish SA-AKI from sepsis patients and was negatively correlated with serum creatinine (Scr), blood urea nitrogen (BUN), cystatin-C (Cys-C), kidney injury molecule-1 (KIM-1), C-reactive protein (CRP), procalcitonin (PCT), and white blood cell (WBC). Low expression of miR-379-5p was correlated with the 28-day survival rate. LPS could inhibit the expression of miR-379-5p in HK-2 cells, inhibit cell viability, and promote the concentration of inflammatory factors TNF-α, IL-1β, and IL-6. Overexpression of miR-379-5p reversed the effect of LPS on HK-2 cells. EDN1 was a direct target gene of miR-379-5p. Overexpression of EDN1 counteracted the protective effect of miR-379-5p overexpression on HK-2 cells. Downregulated serum miR-379-5p had the potential value in diagnosing SA-AKI and forecasting 28-day patient survival. Overexpression of miR-379-5p protected HK-2 cells from LPS-induced injury by targeting and inhibiting EDN1.
如何引用
AMA
Xiaoyu Wang, Hongdong Li, Xianfeng Yu, Mengmeng Li. miR-379-5p serves as a biomarker and regulates sepsis-associated acute kidney injury via targeting EDN1.. BMC immunology. 2026; doi:10.1186/s12865-026-00881-1.
APA
Xiaoyu Wang, Hongdong Li, Xianfeng Yu, Mengmeng Li (2026). miR-379-5p serves as a biomarker and regulates sepsis-associated acute kidney injury via targeting EDN1.. BMC immunology. https://doi.org/10.1186/s12865-026-00881-1
GB/T 7714
Xiaoyu Wang, Hongdong Li, Xianfeng Yu, Mengmeng Li. miR-379-5p serves as a biomarker and regulates sepsis-associated acute kidney injury via targeting EDN1.[J]. BMC immunology, 2026 doi:10.1186/s12865-026-00881-1.
在 PubMed增强版 阅读全文
翻译全文 · AI 文献问答 · PDF 原文下载 · 引用导出