酒精性肝病:当前对细胞机制的认识

Lucy Petagine, Mohammed Gulrez Zariwala, Vinood B Patel
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引用次数: 9

摘要

慢性饮酒引起的酒精性肝病(ALD)是一项重大的全球疾病负担,也是导致死亡的主要原因。酒精滥用在细胞和分子水平上诱导肝细胞发生无数的异常变化。虽然ALD的疾病谱系已被广泛认识,但疾病进展的确切触发因素仍有待充分阐明。氧化应激、线粒体功能障碍、肠道生态失调和免疫系统反应改变在疾病发病机制中发挥重要作用,引发炎症途径的激活和细胞凋亡。尽管最近有许多临床研究表明ALD的治疗选择是有限的,特别是在酒精性肝炎阶段。因此,我们回顾了ALD发病机制中涉及的一些关键途径,并强调了目前治疗患者的试验。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Alcoholic liver disease: Current insights into cellular mechanisms.

Alcoholic liver disease (ALD) due to chronic alcohol consumption is a significant global disease burden and a leading cause of mortality. Alcohol abuse induces a myriad of aberrant changes in hepatocytes at both the cellular and molecular level. Although the disease spectrum of ALD is widely recognized, the precise triggers for disease progression are still to be fully elucidated. Oxidative stress, mitochondrial dysfunction, gut dysbiosis and altered immune system response plays an important role in disease pathogenesis, triggering the activation of inflammatory pathways and apoptosis. Despite many recent clinical studies treatment options for ALD are limited, especially at the alcoholic hepatitis stage. We have therefore reviewed some of the key pathways involved in the pathogenesis of ALD and highlighted current trials for treating patients.

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