J Hepatol:MRG15可能是非酒精性脂肪肝炎的新潜在靶点

2022-08-26 上海营养与健康研究所 上海营养与健康研究所

在肝脏中敲除MRG15后可以显著减缓小鼠NASH发展进程,该研究为NASH治疗提供了潜在的靶点。

在21世纪,非酒精性脂肪肝病(nonalcoholic fatty liver disease, NAFLD)的全球发病率迅速增长,已经成为了最常见的慢性肝病。早期的NAFLD被称为非酒精性脂肪肝(nonalcoholic fatty liver, NAFL),其病理特征为肝脏脂肪变性。当NAFLD发展到后期会成为非酒精性脂肪肝炎(nonalcoholic steatohepatitis, NASH),除了肝脏脂肪变性外还会有肝脏炎症和纤维化出现。到了NASH阶段不及时进行治疗,就有可能继续发展成肝硬化甚至肝细胞癌,严重威胁人类生命健康。NASH发病机制十分复杂,虽然有多款针对NASH的药物在进行临床试验,但目前依旧没有治疗NASH的药物被批准上市,因此深入探究NASH的发病机制和寻找NASH的潜在靶点对于NASH的治疗至关重要。

致死因子4同源蛋白1(Mortality factor 4 like 1, MORF4L1)属于MORF4家族,因为其位于人的第15号染色体上,所以也被称为MRG15。MRG15被认为是一个定位在细胞核的表观调控因子,参与在调控细胞增殖、DNA修复和胚胎发育过程。中国科学院上海营养与健康研究所研究员丁秋蓉团队在前期工作中发现,MRG15可以节律性调控表观染色质重塑和脂质合成,进而促进高脂喂养诱导的小鼠肝脏脂肪变性(Nature metabolism 2020, 2(5):447-460)。然而,MRG15是否可以在NASH发展过程中参与调控炎症和纤维化并不清楚。

近日,该团队等研究人员在Journal of Hepatology上在线发表标题为MRG15 aggravates nonalcoholic steatohepatitis progression through regulating the mitochondrial proteolytic degradation of TUFM的研究论文,发现在NASH发生过程中,炎症因子会增强MRG15的蛋白稳定性,而MRG15会在线粒体外膜与线粒体Tu翻译延伸因子(TUFM)相互作用并下调TUFM的82和91赖氨酸位点乙酰化水平,从而促进TUFM被线粒体ClpXP蛋白酶体降解。肝脏中TUFM的减少会导致线粒体自噬受到抑制、氧化应激增加以及NLRP3炎症小体激活,加重炎症和纤维化。在肝脏中敲除MRG15后可以显著减缓小鼠NASH发展进程,该研究为NASH治疗提供了潜在的靶点。

研究人员首先发现NASH小鼠肝脏和NASH患者肝脏中,MRG15蛋白水平发生上调,进一步探究发现在NASH发展过程中,炎症因子可以通过上调MRG15的乙酰化水平进而增强MRG15的蛋白稳定性。当通过CRISPR技术在小鼠肝脏组织中敲除MRG15后可以显著改善NASH小鼠肝脏脂肪变性、炎症和纤维化情况,表明MRG15在NASH发展过程中发挥重要作用。通过与早期及后期NASH患者肝脏转录组比对分析发现,MRG15敲除后所改变的通路与在NASH患者后期失调的通路有更高的相关性,这些通路主要是炎症和纤维化相关通路,然而炎症和纤维化相关通路中的基因并不是MRG15直接靶向结合的基因,暗示着MRG15很有可能通过发挥独立于表观调控的功能影响炎症和纤维化。

接下来,研究人员通过分离细胞组分发现MRG15不仅定位在细胞核中,还定位在细胞质和线粒体外膜上。通过CoIP-MS寻找MRG15相互作用蛋白发现,MRG15的确和一些线粒体定位蛋白存在相互作用,其中就包括TUFM。TUFM在之前的研究中被发现可以促进线粒体自噬和降低ROS,这对于NASH发展可能会起到保护作用。通过进一步探究发现,MRG15可以通过降低TUFM的82和91赖氨酸位点乙酰化水平进而加速TUFM被线粒体ClpXP蛋白酶体降解。而敲除MRG15后可以通过增强TUFM的蛋白稳定性促进线粒体自噬和降低ROS水平,从而减缓肝细胞损伤。有趣的是,TUFM在NASH患者的肝脏中也表现出明显的降低,并且与MRG15的水平呈现显著负相关,提示该机制同样存在于NASH患者的发病过程中。

为了探究MRG15对NASH的影响是否依赖于TUFM,研究人员在小鼠肝脏中同时敲除了MRG15和TUFM,发现MRG15和TUFM同时敲除后虽然可以改善NASH小鼠的肝脏脂肪变性,但是却不能改善肝脏炎症和纤维化情况,进一步表明MRG15在NASH发展过程中对肝脏脂肪变性的影响是依赖于其表观调控脂合成基因表达的功能,而对炎症和纤维化的影响则是依赖于对TUFM的蛋白稳定性调控。

综上,该研究揭示了MRG15-TUFM轴对简单的肝脏脂肪变性向NASH后期发展过程中所发挥的作用,并且发现该作用不依赖于MRG15的表观重塑功能,为NASH治疗提供了潜在的靶点。

相关研究工作得到营养与健康所公共技术平台和动物平台的支持。

论文链接

MRG15调控TUFM稳定性并促进NASH发展

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    2022-08-27 gwc384
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    2022-08-26 小小医者

    #非酒精性脂肪肝#是世界级难题,目前主要是机制并不清楚,因此,药物开发就成为黑洞!NASH的#新药研发#,是三大黑洞之一!难比登天

    0

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