新医学2026，Vol.57Issue(9)：1003-1011,9.DOI:10.12464/j.issn.0253-9802.2026-0116
LINC01705在代谢功能障碍相关脂肪性肝病中的作用机制研究进展
Research progress on the mechanism of LINC01705 in metabolic dysfunction-associated steatotic liver disease
摘要
Abstract
Metabolic dysfunction-associated steatotic liver disease(MASLD)has become the most common chronic liver disease worldwide,imposing a substantial disease burden.Long non-coding ribonucleic acid(lncRNA)have been demonstrated to be extensively involved in the regulation of lipid metabolism.However,current studies have mainly focused on liver-derived lncRNA,while the mechanism by which adipose tissue-derived lncRNA affects hepatic lipid metabolism through exosome-mediated inter-organ pathways remains unclear.LINC01705 is a newly identified functional lncRNA produced by adipocytes.Under metabolic stress conditions such as high glucose,LINC01705 is packaged into exosomes and delivered to hepatocytes,where it sponges microRNA(miR)-552-3p through a competing endogenous RNA mechanism,thereby relieving the transcriptional repression of liver X receptor α,activating downstream lipogenic pathways,and promoting lipid accumulation in hepatocytes.This article focuses on LINC01705 and systematically reviews its biological characteristics and regulatory mechanisms in the development and progression of MASLD,with particular emphasis on its inter-organ regulatory features of being"adipocyte-derived,exosome-mediated and liver-targeted".The relationship between adipose tissue and the liver and its clinical significance are further explored at the molecular level,with the aim of providing a reference for research in this field.关键词
LINC01705/长链非编码核糖核酸/代谢功能障碍相关脂肪性肝病/脂质沉积/外泌体Key words
LINC01705/Long non-coding ribonucleic acid/Metabolic dysfunction-associated steatotic liver disease/Lipid deposition/Exosome分类
医药卫生引用本文复制引用
李瑞垚,张佳佳,叶新华..LINC01705在代谢功能障碍相关脂肪性肝病中的作用机制研究进展[J].新医学,2026,57(9):1003-1011,9.基金项目
甘肃省青年科技基金(25JRRA1018) （25JRRA1018）
中国儿童生长发育学术交流专项基金(Z-2019-41-2303) （Z-2019-41-2303）
