Obesity is the primary risk factor for the pathogenesis of non-alcoholic fatty liver disease (NAFLD), the worldwide prevalence of which continues to increase dramatically. The liver plays a pivotal role in the maintenance of whole-body lipid and glucose homeostasis. This is mainly mediated by the transcriptional activation of hepatic pathways that promote glucose and lipid production or utilization in response to the nutritional state of the body. However, in the setting of chronic excessive nutrition, the dysregulation of hepatic transcriptional machinery promotes lipid accumulation, inflammation, metabolic stress, and fibrosis, which culminate in NAFLD. In this review, we provide our current understanding of the transcription factors that have been linked to the pathogenesis and progression of NAFLD. Using publicly available transcriptomic data, we outline the altered activity of transcription factors among humans with NAFLD. By expanding this analysis to common experimental mouse models of NAFLD, we outline the relevance of mouse models to the human pathophysiology at the transcriptional level.

中文翻译：

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非酒精性脂肪肝疾病的转录调控。

肥胖是非酒精性脂肪性肝病（NAFLD）发病机理的主要危险因素，其全球流行率持续急剧上升。肝脏在维持全身脂质和葡萄糖体内平衡中起着关键作用。这主要是由肝脏途径的转录激活介导的，该转录途径响应于人体的营养状态而促进葡萄糖和脂质的产生或利用。然而，在长期过度营养的情况下，肝转录机制的失调会促进脂质积累，炎症，代谢应激和纤维化，最终导致NAFLD。在这篇综述中，我们提供了对与NAFLD的发病机理和进展有关的转录因子的最新了解。使用公开的转录组数据，我们概述了NAFLD人群中转录因子活性的改变。通过将这种分析扩展到NAFLD的常见实验小鼠模型，我们在转录水平上概述了小鼠模型与人类病理生理学的相关性。