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本文引用的文献

1
High Expression of Glycolytic Genes in Cirrhosis Correlates With the Risk of Developing Liver Cancer.肝硬化中糖酵解基因的高表达与患肝癌风险相关。
Front Cell Dev Biol. 2018 Oct 31;6:138. doi: 10.3389/fcell.2018.00138. eCollection 2018.
2
PCAF fine-tunes hepatic metabolic syndrome, inflammatory disease, and cancer.PCAF 精细调节肝脏代谢综合征、炎症性疾病和癌症。
J Cell Mol Med. 2018 Dec;22(12):5787-5800. doi: 10.1111/jcmm.13877. Epub 2018 Sep 14.
3
p300/CBP as a Key Nutritional Sensor for Hepatic Energy Homeostasis and Liver Fibrosis.p300/CBP 作为肝脏能量稳态和肝纤维化的关键营养传感器。
Biomed Res Int. 2018 May 15;2018:8168791. doi: 10.1155/2018/8168791. eCollection 2018.
4
Lysine Deacetylases and Regulated Glycolysis in Macrophages.赖氨酸去乙酰化酶和巨噬细胞中的糖酵解调控
Trends Immunol. 2018 Jun;39(6):473-488. doi: 10.1016/j.it.2018.02.009. Epub 2018 Mar 19.
5
The Mitochondrial Acylome Emerges: Proteomics, Regulation by Sirtuins, and Metabolic and Disease Implications.线粒体酰基组学的出现:蛋白质组学、沉默调节蛋白的调节作用,以及代谢和疾病的影响。
Cell Metab. 2018 Mar 6;27(3):497-512. doi: 10.1016/j.cmet.2018.01.016.
6
Posttranslational Modifications of Pyruvate Kinase M2: Tweaks that Benefit Cancer.丙酮酸激酶M2的翻译后修饰:有益于癌症的微调
Front Oncol. 2018 Feb 7;8:22. doi: 10.3389/fonc.2018.00022. eCollection 2018.
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Features and regulation of non-enzymatic post-translational modifications.非酶促翻译后修饰的特点和调控。
Nat Chem Biol. 2018 Feb 14;14(3):244-252. doi: 10.1038/nchembio.2575.
8
Acetylation accumulates PFKFB3 in cytoplasm to promote glycolysis and protects cells from cisplatin-induced apoptosis.乙酰化作用将 PFKFB3 积累在细胞质中,以促进糖酵解,并保护细胞免受顺铂诱导的细胞凋亡。
Nat Commun. 2018 Feb 6;9(1):508. doi: 10.1038/s41467-018-02950-5.
9
Synergistic interaction of fatty acids and oxysterols impairs mitochondrial function and limits liver adaptation during nafld progression.脂肪酸和氧化固醇的协同作用会损害线粒体功能,并限制非酒精性脂肪性肝病进展过程中的肝脏适应能力。
Redox Biol. 2018 May;15:86-96. doi: 10.1016/j.redox.2017.11.016. Epub 2017 Dec 5.
10
Pyruvate dehydrogenase kinase 4 mediates lipogenesis and contributes to the pathogenesis of nonalcoholic steatohepatitis.丙酮酸脱氢酶激酶4介导脂肪生成并促进非酒精性脂肪性肝炎的发病机制。
Biochem Biophys Res Commun. 2018 Jan 1;495(1):582-586. doi: 10.1016/j.bbrc.2017.11.054. Epub 2017 Nov 9.

酶和非酶蛋白乙酰化控制肝脏疾病中的糖酵解过程。

Enzymatic and nonenzymatic protein acetylations control glycolysis process in liver diseases.

机构信息

Department of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan, China.

出版信息

FASEB J. 2019 Nov;33(11):11640-11654. doi: 10.1096/fj.201901175R. Epub 2019 Aug 1.

DOI:10.1096/fj.201901175R
PMID:31370704
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6902721/
Abstract

Impaired glycolysis has pathologic effects on the occurrence and progression of liver diseases, and it appears that glycolysis is increased to different degrees in different liver diseases. As an important post-translational modification, reversible lysine acetylation regulates almost all cellular processes, including glycolysis. Lysine acetylation can occur enzymatically with acetyltransferases or nonenzymatically with acetyl-coenzyme A. Accompanied by the progression of liver diseases, there seems to be a temporal and spatial variation between enzymatic and nonenzymatic acetylations in the regulation of glycolysis. Here, we summarize the most recent findings on the functions and targets of acetylation in controlling glycolysis in the different stages of liver diseases. In addition, we discuss the differences and causes between enzymatic and nonenzymatic acetylations in regulating glycolysis throughout the progression of liver diseases. Then, we review these new discoveries to provide the potential implications of these findings for therapeutic interventions in liver diseases.-Li, J., Wang, T., Xia, J., Yao, W., Huang, F. Enzymatic and nonenzymatic protein acetylations control glycolysis process in liver diseases.

摘要

糖酵解受损对肝脏疾病的发生和发展有病理影响,似乎不同的肝脏疾病中糖酵解的增加程度不同。作为一种重要的翻译后修饰,可逆赖氨酸乙酰化调节着几乎所有的细胞过程,包括糖酵解。赖氨酸乙酰化可以通过乙酰转移酶酶促发生,也可以通过乙酰辅酶 A 非酶促发生。随着肝脏疾病的进展,在糖酵解的调节中,酶促和非酶促乙酰化之间似乎存在时空变化。在这里,我们总结了最近关于在不同阶段的肝脏疾病中,乙酰化对控制糖酵解的功能和靶标的发现。此外,我们还讨论了在整个肝脏疾病进展过程中,酶促和非酶促乙酰化在调节糖酵解方面的差异和原因。然后,我们回顾了这些新发现,为这些发现对肝脏疾病治疗干预的潜在意义提供了参考。