长链非编码rna在代谢功能障碍相关脂肪变性肝病和纤维化发病机制中的作用

eGastroenterology Pub Date : 2024-11-01 Epub Date: 2024-11-18 DOI:10.1136/egastro-2024-100115
Henry Wade, Kaichao Pan, Bingrui Zhang, Wenhua Zheng, Qiaozhu Su
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引用次数: 0

摘要

代谢功能障碍相关脂肪性肝病(MASLD),以前被称为非酒精性脂肪性肝病,包括广泛的肝脏代谢紊乱,主要特征是肝脂质代谢紊乱、肝脂质积累和脂肪变性。严重的MASLD可能发展为代谢功能障碍相关的脂肪性肝炎,以肝脏炎症、肝细胞球囊变性、肝星状细胞(hsc)活化和纤维化为特征。它可能进一步发展为肝细胞癌。在肝脏中,长链非编码rna (lncRNAs)在MASLD和肝纤维化的不同阶段靶向肝细胞、hsc和Kupffer细胞的多种代谢途径。在这项研究中,我们概述了lncRNAs在MASLD和肝纤维化发病机制中的潜在作用,包括通过调节新生脂质合成、脂肪酸β-氧化、脂肪毒性、氧化应激、代谢性炎症、雷帕霉素信号传导的哺乳动物靶点、细胞凋亡、泛素化和纤维化。我们批判性地评估了在MASLD和肝纤维化的人类参与者和动物模型中研究lncRNA、microRNA和肝损伤关键介质之间复杂相互作用的文献报告。我们还强调了lncrna在慢性肝脏疾病中的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanistic role of long non-coding RNAs in the pathogenesis of metabolic dysfunction-associated steatotic liver disease and fibrosis.

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously referred to as non-alcoholic fatty liver disease, encompasses a broad range of hepatic metabolic disorders primarily characterised by the disruption of hepatic lipid metabolism, hepatic lipid accumulation and steatosis. Severe cases of MASLD might progress to metabolic dysfunction-associated steatohepatitis, characterised by hepatic inflammation, hepatocyte ballooning degeneration, activation of hepatic stellate cells (HSCs) and fibrogenesis. It may further progress to hepatocellular carcinoma. In the liver, long non-coding RNAs (lncRNAs) target multiple metabolic pathways in hepatocytes, HSCs, and Kupffer cells at different stages of MASLD and liver fibrosis. In this study, we overview recent findings on the potential role of lncRNAs in the pathogenesis of MASLD and liver fibrosis via modulation of de novo lipid synthesis, fatty acid β-oxidation, lipotoxicity, oxidative stress, metabolic inflammation, mammalian target of rapamycin signalling, apoptosis, ubiquitination and fibrogenesis. We critically assess the literature reports that investigate the complex interplay between lncRNA, microRNA and key mediators in liver injury, in both human participants and animal models of MASLD and liver fibrosis. We also highlight the therapeutic potential of lncRNAs in chronic liver diseases.

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