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Background <p>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).</p> Methods <p>Serum miR<b>-</b>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.</p> Results <p>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.</p> Conclusions <p>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.</p>

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miR-379-5p serves as a biomarker and regulates sepsis-associated acute kidney injury via targeting EDN1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月3日

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  • Xiaoyu Wang,
  • Hongdong Li,
  • Xianfeng Yu,
  • Mengmeng Li

摘要

Background

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).

Methods

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.

Results

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.

Conclusions

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.