Central European Journal of Immunology
eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
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abstract:
Original paper

lncRNA FENDRR targets miR-3614-5p to promote sepsis-induced acute kidney injury via the pro-inflammatory response

Quanan He
1
,
Yiqing Li
2
,
Yanping Peng
3
,
Xiaodan Sun
3
,
Yao Ma
3
,
Xusheng Yang
3
,
Yang Zhao
3
,
Yunxiao Jia
3
,
Yunxing Guo
3
,
Jianping Yi
4

  1. Department of Emergency, Wuhan Brain Hospital, General Hospital of the Yangtze River Shipping, China
  2. Department of Intensive Care Medicine, Xi’an Power Central Hospital of Genertec Guozhong Healthcare Limited Company, China
  3. Department of Nephrology, Beijing Rehabilitation Hospital, Capital Medical School, China
  4. Emergency Department, The 940th Hospital of Joint Logistic Support Force of Chinese People’s Liberation Army, China
Cent Eur J Immunol 2025; 50
DOI: https://doi.org/10.5114/ceji.2025.155094
Online publish date: 2025/10/16
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Introduction
Acute kidney injury (AKI) raises mortality rates in septic patients. This study investigated the relationship between lncRNA FENDRR and miR-3614-5p, aiming to examine FENDRR’s clinical significance in sepsis-induced AKI and identify new diagnostic biomarkers.

Material and methods
Eighty-five patients with sepsis-induced AKI and 90 patients with sepsis were included. ROC curve and multivariate logistic analysis were performed to assess the diagnostic value of FENDRR and risk factors, respectively. The binding between FENDRR and miR-3614-5p was detected by the dual-luciferase reporter assay. An inflammatory cell model was constructed using lipopolysaccharide (LPS) to verify the effects of FENDRR on cell function and inflammation.

Results
FENDRR was down-regulated and miR-3614-5p was up-regulated in AKI patients, with a negative correlation and target-binding relationship. FENDRR has potential diagnostic value in differentiating between patients with sepsis-induced AKI and those with sepsis. FENDRR is a risk factor for sepsis-induced AKI. Procalcitonin (PCT), blood urea nitrogen (BUN), serum creatinine (SCr), Acute Physiology and Chronic Health Evaluation II (APACHE II), Sequential Organ Failure Assessment (SOFA), lactate, and length of hospital stay were positively correlated with FENDRR in AKI patients. Silencing of FENDRR alleviated the LPS-induced increase in MDA content, reactive oxygen species (ROS), levels of inflammatory factors, and renal injury markers in HK-2 cells while mitigating the LPS-induced increase in apoptosis rate and decrease in cellular activity.

Conclusions
FENDRR serves as a biomarker for sepsis-induced AKI. FENDRR inhibits miR-3614-5p to regulate cellular inflammation and oxidative damage and plays a crucial role in the pathogenesis of sepsis-induced AKI.

keywords:

sepsis, acute kidney injury, cellular inflammation, FENDRR
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