Laboratory of Hygienic Chemistry, Department of Health Science and Hygiene, Daiichi University of Pharmacy.
Department of Veterinary and Biomedical Sciences and the Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University.
Biol Pharm Bull. 2021;44(11):1598-1606. doi: 10.1248/bpb.b21-00486.
Excessive, chronic alcohol consumption can lead to alcoholic liver disease. The etiology of alcoholic liver disease is multifactorial and is influenced by alterations in gene expression and changes in fatty acid metabolism, oxidative stress, and insulin resistance. These events can lead to steatosis, fibrosis, and eventually to cirrhosis and liver cancer. Many of these functions are regulated by peroxisome proliferator-activated receptors (PPARs). Thus, it is not surprising that PPARs can modulate the mechanisms that cause alcoholic liver disease. While the roles of PPARα and PPARγ are clearer, the role of PPARβ/δ in alcoholic liver disease requires further clarification. This review summarizes the current understanding based on recent studies that indicate that PPARβ/δ can likely be targeted for the treatment and/or the prevention of alcoholic liver disease.
过量、长期饮酒会导致酒精性肝病。酒精性肝病的病因是多因素的，受基因表达改变和脂肪酸代谢、氧化应激和胰岛素抵抗的影响。这些事件可导致脂肪变性、纤维化，最终导致肝硬化和肝癌。这些功能中的许多都受过氧化物酶体增殖物激活受体 (PPARs) 的调节。因此，PPARs 可以调节导致酒精性肝病的机制并不奇怪。虽然 PPARα 和 PPARγ 的作用更为明确，但 PPARβ/δ 在酒精性肝病中的作用需要进一步阐明。这篇综述总结了基于最近研究的现有认识，这些研究表明，PPARβ/δ 可能是治疗和/或预防酒精性肝病的一个潜在靶点。
