TRIM67 缺失可减轻肥胖诱导的非酒精性脂肪性肝病的进展。
Loss of TRIM67 Attenuates the Progress of Obesity-Induced Non-Alcoholic Fatty Liver Disease.
机构信息
Laboratory of Experimental Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China.
Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China.
出版信息
Int J Mol Sci. 2022 Jul 5;23(13):7475. doi: 10.3390/ijms23137475.
Obesity is considered as a major cause for the development and progress of non-alcoholic fatty liver disease (NAFLD), which is one of the most prevalent chronic liver diseases worldwide. However, molecular mechanisms that implicate in obesity-driven pathophysiology of NAFLD are not well defined. Here, we report a tripartite motif (TRIM) protein family member-TRIM67-that is hardly expressed in liver but is inducible on obese conditions. Enhanced expression of TRIM67 activates hepatic inflammation to disturb lipid metabolic homeostasis and promote the progress of NAFLD induced by obesity, while the deficiency in TRIM67 is protective against these pathophysiological processes. Finally, we show that the important transcription coactivator PGC-1α implicates in the response of hepatic TRIM67 to obesity.
肥胖被认为是导致非酒精性脂肪性肝病（NAFLD）发展和进展的主要原因，NAFLD 是全球最常见的慢性肝病之一。然而，涉及肥胖驱动的 NAFLD 病理生理学的分子机制尚未明确。在这里，我们报告了一个三基序（TRIM）蛋白家族成员-TRIM67-在肝脏中几乎不表达，但在肥胖条件下可诱导表达。TRIM67 的增强表达会激活肝脏炎症，扰乱脂质代谢平衡，并促进肥胖引起的 NAFLD 进展，而 TRIM67 的缺乏则对这些病理生理过程具有保护作用。最后，我们表明，重要的转录共激活因子 PGC-1α 涉及肝脏 TRIM67 对肥胖的反应。
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