Abstract
Sepsis is a severe organ dysfunction disease, usually accompanied by acute kidney injury (AKI). miR-29b-3p was inhibited in sepsis-induced AKI, while its role in AKI was unclear. Therefore, this study determined the role of miR-29b-3p in sepsis-induced AKI, and investigated its underlying mechanism. In this study, the AKI model was established through injecting with lipopolysaccharides (LPS) intraperitoneally. In LPS challenged mice, serum blood urea nitrogen and creatinine were increased, and renal tissues pathological damage was induced. Besides, miR-29b-3p was declined in LPS-induced AKI mice and podocytes. In addition, HDAC4 was elevated in LPS-treated podocytes. Furthermore, upregulated miR-29b-3p attenuated LPS-induced mice podocyte injury, and HDAC4 was identified as a direct target of miR-29b-3p. Moreover, overexpression of miR-29b-3p attenuated LPS-induced AKI in mice. In conclusion, miR-29b-3p was inhibited in LPS-induced AKI. Downregulation of miR-29b-3p aggravated podocyte injury through targeting HDAC4 in LPS-induced AKI. miR-29b-3p may act as a valuable target for AKI therapy.