移动端阅览
中南大学湘雅二医院消化内科,中南大学消化病研究中心,湖南省消化疾病临床医学研究中心,长沙 410011
杨雨晴,Email: yyyangyuqing111@163.com, ORCID: 0009-0001-7894-0460
谭玉勇,副主任医师,Email: tanyuyong@csu.edu.cn, ORCID: 0000-0002-0571-3136
收稿:2025-05-08,
纸质出版:2026-02-28
杨雨晴, 余美红, 刘德良, 谭玉勇. 组蛋白去乙酰化酶与酒精相关性肝病[J]. 中南大学学报(医学版), 2026, 51(2): 202-212.
YANG Yuqing, YU Meihong, LIU Deliang, TAN Yuyong. Histone deacetylases and alcohol-related liver disease[J]. Journal of Central South University. Medical Science, 2026, 51(2): 202-212.
杨雨晴, 余美红, 刘德良, 谭玉勇. 组蛋白去乙酰化酶与酒精相关性肝病[J]. 中南大学学报(医学版), 2026, 51(2): 202-212. DOI:10.11817/j.issn.1672-7347.2026.250225.
YANG Yuqing, YU Meihong, LIU Deliang, TAN Yuyong. Histone deacetylases and alcohol-related liver disease[J]. Journal of Central South University. Medical Science, 2026, 51(2): 202-212. DOI:10.11817/j.issn.1672-7347.2026.250225.
酒精相关性肝病(alcohol-related liver disease,ALD)是长期大量饮酒导致的一种常见慢性肝病。早期可无任何症状或表现为轻症酒精性脂肪肝,随后可演变为以肝脏炎症为特征的亚临床脂肪性肝炎,进一步发展为纤维化、肝硬化,晚期严重时可诱发肝功能衰竭和肝细胞癌。目前,戒酒是ALD干预的核心策略,但受制于患者依从性及社会环境等因素,常需联合药物治疗。组蛋白去乙酰化酶(histone deacetylase,HDAC)是蛋白质翻译后修饰的关键功能性催化酶,可通过影响脂质代谢、炎症反应及纤维化等过程,参与ALD的发生和发展,可作为ALD治疗的潜在靶点。多种HDAC相关激动剂和抑制剂在ALD治疗中有一定应用前景,但其亚型特异性作用及临床应用价值仍需进一步明确。对HDAC及其激动剂或抑制剂在ALD中的作用进行系统概括,可为进一步探讨ALD发生、发展机制及推动ALD的精准干预提供思路。
Alcohol-related liver disease (ALD) is a common chronic liver disease caused by prolonged excessive alcohol consumption. It may initially be asymptomatic or manifest as mild alcoholic fatty liver
then progress to subclinical steatohepatitis characterized by hepatic inflammation
and eventually develop into fibrosis
cirrhosis
liver failure
or even hepatocellular carcinoma. Although alcohol abstinence remains the primary strategy for ALD management
its effectiveness is often limited by patient adherence and social factors
making combined pharmacological intervention necessary in many cases. Histone deacetylase (HDAC)
which is a key enzyme involved in post-translational protein modification
have been implicated in the pathogenesis and progression of ALD through their regulation of lipid metabolism
inflammatory responses
and fibrosis
and are therefore considered promising therapeutic targets. Various HDAC-related agonists and inhibitors have shown therapeutic potential in ALD
but their subtype-specific roles and clinical relevance remain to be fully elucidated. This review systematically summarizes the roles of HDAC and their agonists or inhibitors in ALD
in order to provide insight into the mechanisms of ALD progression and to support the development of precise therapeutic strategies and clinical translation.
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