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脂肪性肝病(fattyliverdisease,FLD)具有多样病因和多种形态谱,包括单纯性脂肪肝、脂肪性肝炎、脂肪性肝纤维化,以及其进一步进展为肝硬化和肝细胞癌。根据病因FLD被分成两大类:酒精性脂肪性肝病(alcoholicfattyliverdisease,AFLD)和非酒精性脂肪性肝病(nonalcoholicfattyliverdisease,NAFLD)。两者的病理变化过程没有明显差异,提示两者可能具有一个复杂但共同的发病机制。过氧化物酶体增殖物激活受体(peroxisomeproliferator-activatedreceptors,PPARs)由Isseman等在1990年研究小鼠肝脏cDNA文库时首先发现,是一类由配体激活的核转录因子,属于核受体超家族成员。近年研究发现PPARs的一个亚型PPARα具有调节脂肪代谢和调节炎症、免疫以及细胞分化等作用,从而参与脂肪性肝病的发病机制,本文就此做一综述。
Fatty liver disease (FLD) has a diverse spectrum of etiologies and morphologies, including simple fatty liver, steatohepatitis, fatty liver fibrosis, and its further progression to cirrhosis and hepatocellular carcinoma. According to the cause of FLD is divided into two categories: alcoholic fatty liver disease (alcoholicfattyliverdisease, AFLD) and non-alcoholic fatty liver disease (NAFLD). Pathological changes between the two no significant difference, suggesting that the two may have a complex but common pathogenesis. Peroxisome proliferator-activated receptors (PPARs) were first discovered by Isseman et al in the study of mouse liver cDNA library in 1990. They are a class of ligand-activated nuclear transcription factors that belong to nuclear receptor super family members. Recent studies have found that PPARα, a subtype of PPARs, is involved in the pathogenesis of fatty liver disease by regulating the metabolism of fat and regulating inflammation, immunity and cell differentiation.