DEAD-Box Helicase 17 exacerbates non-alcoholic steatohepatitis via transcriptional repression of cyp2c29, inducing hepatic lipid metabolism disorder and eliciting the activation of M1 macrophages.

Deng NingJie JinYuanyuan FangPengcheng DuChaoyi YuanJin ChenQibo HuangKun ChengJie MoLei XuHui GuoMia Jiming YangXiaoping ChenHuifang LiangBixiang ZhangWan-Guang Zhang

Published in: Clinical and translational medicine (2024)

These results imply that DDX17 is involved in NASH development by promoting lipid accumulation in hepatocytes, inducing the activation of M1 macrophages, subsequent inflammatory responses and fibrosis through the transcriptional repression of Cyp2c29 in mice. Therefore, DDX17 holds promise as a potential drug target for the treatment of NASH.

Keyphrases

heat shock protein
transcription factor
liver injury
gene expression
drug induced
big data
emergency department
liver fibrosis
type diabetes
high fat diet induced
metabolic syndrome
fatty acid
oxidative stress
risk assessment
combination therapy
insulin resistance
adverse drug
wild type