Department of Pharmacology, Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Department of Pharmacology, Jiangsu Key Laboratory of Therapeutic Material of Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Signal Transduct Target Ther. 2020 Dec 4;5(1):280. doi: 10.1038/s41392-020-00349-7.
As one of the bicyclic metabolic pathways of one-carbon metabolism, methionine metabolism is the pivot linking the folate cycle to the transsulfuration pathway. In addition to being a precursor for glutathione synthesis, and the principal methyl donor for nucleic acid, phospholipid, histone, biogenic amine, and protein methylation, methionine metabolites can participate in polyamine synthesis. Methionine metabolism disorder can aggravate the damage in the pathological state of a disease. In the occurrence and development of chronic liver diseases (CLDs), changes in various components involved in methionine metabolism can affect the pathological state through various mechanisms. A methionine-deficient diet is commonly used for building CLD models. The conversion of key enzymes of methionine metabolism methionine adenosyltransferase (MAT) 1 A and MAT2A/MAT2B is closely related to fibrosis and hepatocellular carcinoma. In vivo and in vitro experiments have shown that by intervening related enzymes or downstream metabolites to interfere with methionine metabolism, the liver injuries could be reduced. Recently, methionine supplementation has gradually attracted the attention of many clinical researchers. Most researchers agree that adequate methionine supplementation can help reduce liver damage. Retrospective analysis of recently conducted relevant studies is of profound significance. This paper reviews the latest achievements related to methionine metabolism and CLD, from molecular mechanisms to clinical research, and provides some insights into the future direction of basic and clinical research.
蛋氨酸代谢是一碳代谢的双环代谢途径之一,是连接叶酸循环与转硫途径的枢纽。除了是谷胱甘肽合成的前体,也是核酸、磷脂、组蛋白、生物胺和蛋白质甲基化的主要甲基供体外,蛋氨酸代谢物还可以参与多胺合成。蛋氨酸代谢紊乱会加重疾病病理状态下的损伤。在慢性肝病(CLD)的发生和发展中,蛋氨酸代谢中各种成分的变化可以通过多种机制影响病理状态。蛋氨酸缺乏饮食通常用于建立 CLD 模型。蛋氨酸代谢关键酶蛋氨酸腺苷转移酶(MAT)1A 和 MAT2A/MAT2B 的转换与纤维化和肝细胞癌密切相关。体内和体外实验表明,通过干预相关酶或下游代谢物来干扰蛋氨酸代谢,可以减轻肝损伤。最近,蛋氨酸补充逐渐引起了许多临床研究人员的关注。大多数研究人员认为,充足的蛋氨酸补充可以帮助减轻肝损伤。对最近进行的相关研究进行回顾性分析具有重要意义。本文综述了蛋氨酸代谢与 CLD 的最新研究成果,从分子机制到临床研究,为基础和临床研究的未来方向提供了一些见解。