脂肪肝
生物
脂质代谢
小RNA
酒精性肝病
肝细胞
酒精性脂肪肝
癌症研究
细胞生物学
体外
内科学
疾病
内分泌学
生物化学
基因
肝硬化
医学
作者
Jiayin Li,Haixu Song,Zimeng Chen,Yang Qiumin,Zheming Yang,Chenghui Yan,Chongbin Zhong
标识
DOI:10.1016/j.yexcr.2023.113631
摘要
Non-alcoholic fatty liver disease (NAFLD) is one of the main causes of liver disease that has reached its last stage. Over the past few years, evidence for miRNAs' centrality in NAFLD pathogenesis has accumulated. According to some studies, miR-574-5p plays a role in lipid metabolism. However, research on the relationship between miR-574-5p and NAFLD is lacking. For in vivo experiments, we induced the NAFLD mice model with a high-fat diet (HFD). AgomiR-574-5p was injected intravenously into HFD-fed mice for eight weeks, and qPCR was used to identify the expression of miR-574-5p in the serum. In in vitro experiments, The treatment of L-O2 cells with a miR-574-5p mimic resulted in a significant reduction in lipid deposition, suggesting that miR-574-5p can inhibit lipid accumulation and lipid formation induced by OA. The dual-luciferase reporter gene assay revealed that miR-574-5p targets the 3' UTR region of HOXC6 directly. We discovered that OA-induced lipid accumulation in hepatocytes might be mediated through the miR-574-5p-HOXC6 signaling axis. Additional research is required in order to determine the specific mechanism by which HOXC6 downstream pathways are involved in the miR-574-5p induced lipid uptake.
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