酒精性肝病的发病机制：最新研究进展。
Pathogenesis of Alcoholic Liver Disease: An Update.
机构信息
Department of Gastroenterology, Baylor College of Medicine, 6620 Main Street, Suite 1450, Houston, TX 77030, USA.
Department of Surgery, Division of Abdominal Transplantation, Baylor College of Medicine, 6620 Main Street, Suite 1450, Houston, TX 77030, USA.
出版信息
Clin Liver Dis. 2019 Feb;23(1):71-80. doi: 10.1016/j.cld.2018.09.006.
Apart from the classic knowledge that ethanol mediates its hepatotoxicity through its metabolism to acetaldehyde, a well-known hepatotoxic molecule, recent research has elucidated several key mechanisms that potentiate ethanol's damage to the liver parenchyma, such as generation of free radicals, activation of Kupffer cells, and alterations to the human bacterial and fungal microbiome. Genetic studies have suggested the role of PNPLA3 and TM6SF2 gene mutations in the progression of alcoholic liver disease.
除了经典的知识，即乙醇通过代谢为乙醛（一种众所周知的肝毒性分子）介导其肝毒性外，最近的研究还阐明了几种增强乙醇对肝实质损伤的关键机制，如自由基的产生、枯否细胞的激活以及人类细菌和真菌微生物组的改变。遗传研究表明 PNPLA3 和 TM6SF2 基因突变在酒精性肝病的进展中起作用。
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