表观遗传学在瘦型非酒精性脂肪性肝病中的作用及临床应用前景
DOI: 10.12449/JCH250624
Role and clinical application prospect of epigenetics in lean nonalcoholic fatty liver disease
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摘要: 表观遗传学机制在非酒精性脂肪性肝病(NAFLD)的发生、发展中扮演着至关重要的角色,尤其是在瘦人群体中,相关表观遗传学机制的研究为揭示NAFLD的潜在病因和治疗策略提供了新的线索和方向。本文介绍了近年表观遗传学在瘦型NAFLD发展中的作用,分析了瘦型NAFLD表观遗传学方面的最新研究进展,简述了表观遗传学的基本概念,包括DNA甲基化、组蛋白修饰和非编码RNA调控,并探讨了表观遗传学改变如何影响瘦型NAFLD的发病机制、疾病进展以及治疗策略。Abstract: Epigenetic mechanisms play a crucial role in the development and progression of nonalcoholic fatty liver disease (NAFLD), especially among lean individuals. The research on related epigenetic mechanisms has provided new clues and directions for revealing the underlying causes and treatment strategies of NAFLD. This article introduces the role of epigenetics in the development and progression of NAFLD among lean individuals in recent years, analyzes the latest research advances in the epigenetics of NAFLD in this population, and briefly describes the basic concepts of epigenetics, including DNA methylation, histone modifications, and non-coding RNA regulation. This article also discusses how epigenetic alterations impact the pathogenesis, disease progression, and treatment strategies of NAFLD in lean individuals.
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Key words:
- Non-alcoholic Fatty Liver Disease /
- Epigenomics /
- Pathologic Processes
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表 1 非瘦型NAFLD与瘦型NAFLD两种分型的区别
Table 1. The difference between the two types of non-lean NAFLD and lean NAFLD
项目 非瘦型NAFLD 瘦型NAFLD 1型 瘦型NAFLD 2型 BMI(亚洲人群标准) >27.5 kg/m2 <23 kg/m2,但以腰围或其他身
体成分可能衡量为肥胖BMI处于瘦人范畴,且无
内脏肥胖主要发病机制 胰岛素抵抗和脂肪代谢紊乱、氧化应激和脂质
过氧化、炎症反应和免疫失调、肠道菌群失调内脏肥胖和胰岛素抵抗 单基因疾病导致 主要病理改变 单纯脂肪肝:肝细胞大量脂滴积累,无明显肝细
胞损伤;NASH:肝细胞明显损伤和炎细胞浸润;
肝纤维化和肝硬化:肝细胞正常结构严重破坏,
假小叶形成,伴有广泛肝纤维化脂肪变性、(严重)代谢异常:血
脂异常、空腹血糖上升等,易出
现炎症和肝纤维化,进而发展
为肝硬化脂肪变性(较1型轻)、代
谢异常(较1型轻):血脂
异常、空腹血糖上升等,遗
传基因变异 -
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