OBJECTIVE AND DESIGN Nowadays, sepsis-induced acute kidney injury (AKI) has gradually become a global problem for its high incidence and increasing mortality. Previous study has reported lncRNA ENST00000452391.1 in sepsis patients. However, its potential biological function and downstream molecular mechanism are still mysterious. METHODS AND RESULTS: Our study found that it was upregulated in sepsis-induced AKI patients, so it was identified as "sepsis-induced kidney injury associated transcript 1 (SIKIAT1)". We used lipopolysaccharide (LPS) stimulated HK-2 cells as an in vitro model to demonstrated that SIKIAT1 acts as a ceRNA for miR-96-3p to enhance FOXA1 expression and promote HK-2 cell apoptosis. CONCLUSION Therefore, it could be a potential biomarker and therapeutic target for sepsis-induced AKI in the development of disease.

中文翻译：

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SIKIAT1 / miR-96 / FOXA1轴通过诱导细胞凋亡来调节败血症诱导的肾脏损伤。

目的和设计如今，败血症诱导的急性肾损伤（AKI）由于其高发病率和高死亡率而逐渐成为全球性问题。先前的研究已报道败血症患者的lncRNA ENST00000452391.1。然而，其潜在的生物学功能和下游分子机制仍是未知的。方法和结果：我们的研究发现，它在败血症诱导的AKI患者中被上调，因此被鉴定为“败血症诱导的肾损伤相关转录本1（SIKIAT1）”。我们使用脂多糖（LPS）刺激的HK-2细胞作为体外模型，以证明SIKIAT1作为miR-96-3p的ceRNA增强FOXA1表达并促进HK-2细胞凋亡。结论因此，它可能是脓毒症诱发的AKI在疾病发展中的潜在生物标志物和治疗靶标。