Shijun Lu1, Haibin Wu2, Jianhua Xu3, Zhaofeng He4, Haiyan Li3, Chao Ning3. 1. Department of Critical Care Medicine, Shandong Province Linyi Central Hospital, Shandong, China. lushijun2020@126.com. 2. Department of Critical Care Medicine, The Affiliated Hospital of Guangdong Medical College, Guangdong, China. 3. Department of Critical Care Medicine, Shandong Province Linyi Central Hospital, Shandong, China. 4. Department of Critical Care Medicine, Shandong Province Juxian People's Hospital, Shandong, China.
Abstract
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.
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 sepsispatients. 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.