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天然脂噬调节剂在代谢功能障碍相关脂肪性肝病中的新作用。

Emerging role of natural lipophagy modulators in metabolic dysfunction-associated steatotic liver disease.

机构信息

Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, Egypt; Department of Pharmacology & Biochemistry, Faculty of Pharmacy, The British University in Egypt, El Sherouk, Cairo, Egypt.

Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, Egypt.

出版信息

Nutrition. 2024 Oct;126:112517. doi: 10.1016/j.nut.2024.112517. Epub 2024 Jun 11.

DOI:10.1016/j.nut.2024.112517
PMID:39146583
Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease (NAFLD), is a seriously increasing liver disorder affecting nearly 32% of adults globally. Hepatic triglycerides (TG) accumulation is the hallmark of MASLD, which results from dysregulated lipid and fatty acid uptake, increased de novo lipogenesis (DNL), and decreased lipid removal. More recently, selective autophagy of lipid droplets (LDs), termed lipophagy, has emerged to be closely associated with disrupted hepatic lipid homeostasis. Recent studies have indicated that a series of natural products have shown promise as an alternative approach in attenuating MASLD via regulating lipophagy in vivo and in vitro. Therefore, lipophagy could be a new approach for natural products to be used to improve MASLD. This article aims to provide a comprehensive overview on the interrelationship between dysregulated lipid metabolism, lipophagy, and MASLD pathogenesis. In addition, the role of some natural products as lipophagy modulators and their impact on MASLD will be discussed.

摘要

代谢相关脂肪性肝病(MASLD),以前称为非酒精性脂肪性肝病(NAFLD),是一种严重的肝脏疾病,全球近 32%的成年人受其影响。肝内甘油三酯(TG)堆积是 MASLD 的标志,这是由于脂质和脂肪酸摄取失调、从头合成(DNL)增加和脂质清除减少所致。最近,脂质滴(LDs)的选择性自噬,即脂噬,已被证明与肝脏脂质代谢失衡密切相关。最近的研究表明,一系列天然产物通过调节体内和体外的脂噬,在减轻 MASLD 方面显示出良好的应用前景。因此,脂噬可能成为天然产物改善 MASLD 的一种新方法。本文旨在全面概述脂质代谢失调、脂噬与 MASLD 发病机制之间的相互关系。此外,还将讨论一些天然产物作为脂噬调节剂的作用及其对 MASLD 的影响。

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引用本文的文献

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Antioxidants (Basel). 2025 Jul 24;14(8):908. doi: 10.3390/antiox14080908.