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非酒精性脂肪性肝病中铁代谢与铁死亡:我们的下一步是什么?

Iron metabolism and ferroptosis in nonalcoholic fatty liver disease: what is our next step?

机构信息

Munich Medical Research School, Ludwig Maximilian University of Munich, Munich, Germany.

Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Nanchang Medical College, Jiangxi Provincial People's Hospital, Nanchang, People's Republic of China.

出版信息

Am J Physiol Endocrinol Metab. 2024 Jun 1;326(6):E767-E775. doi: 10.1152/ajpendo.00260.2023. Epub 2024 Mar 20.

DOI:10.1152/ajpendo.00260.2023
PMID:38506752
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11376490/
Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease with increasing prevalence worldwide. NAFLD could develop from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH), NASH-related fibrosis, cirrhosis, and even hepatocellular carcinoma. However, the mechanism of NAFLD development has not yet been fully defined. Recently, emerging evidence shows that the dysregulated iron metabolism marked by elevated serum ferritin, and ferroptosis are involved in the NAFLD. Understanding iron metabolism and ferroptosis can shed light on the mechanisms of NAFLD development. Here, we summarized studies on iron metabolism and the ferroptosis process involved in NAFLD development to highlight potential medications and therapies for treating NAFLD.

摘要

非酒精性脂肪性肝病(NAFLD)是最常见的慢性肝病,全球患病率呈上升趋势。NAFLD 可由单纯性肝脂肪变性发展为非酒精性脂肪性肝炎(NASH)、NASH 相关纤维化、肝硬化,甚至肝细胞癌。然而,NAFLD 的发病机制尚未完全明确。最近的研究表明,铁代谢失调标志着血清铁蛋白升高,铁死亡参与了 NAFLD 的发生。了解铁代谢和铁死亡可以揭示 NAFLD 发病机制。本文总结了 NAFLD 发病过程中铁代谢和铁死亡的相关研究,以强调治疗 NAFLD 的潜在药物和治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2f4/11376490/f9df1e6603b9/ajpendo.00260.2023_f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2f4/11376490/0deebe4c9256/ajpendo.00260.2023_f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2f4/11376490/1be0f71930ca/ajpendo.00260.2023_f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2f4/11376490/f9df1e6603b9/ajpendo.00260.2023_f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2f4/11376490/0deebe4c9256/ajpendo.00260.2023_f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2f4/11376490/1be0f71930ca/ajpendo.00260.2023_f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2f4/11376490/f9df1e6603b9/ajpendo.00260.2023_f003.jpg

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H3K9 trimethylation dictates neuronal ferroptosis through repressing .H3K9 三甲基化通过抑制. 来控制神经元铁死亡。
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