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S‐adenosylmethionine: A metabolite critical to the regulation of autophagy
Cell Proliferation ( IF 5.9 ) Pub Date : 2020-10-08 , DOI: 10.1111/cpr.12891
Yang Ouyang 1 , Qi Wu 1 , Juanjuan Li 1 , Si Sun 2 , Shengrong Sun 1
Affiliation  

Autophagy is a mechanism that enables cells to maintain cellular homeostasis by removing damaged materials and mobilizing energy reserves in conditions of starvation. Although nutrient availability strongly impacts the process of autophagy, the specific metabolites that regulate autophagic responses have not yet been determined. Recent results indicate that S‐adenosylmethionine (SAM) represents a critical inhibitor of methionine starvation–induced autophagy. SAM is primarily involved in four key metabolic pathways: transmethylation, transsulphuration, polyamine synthesis and 5′‐deoxyadenosyl 5′‐radical–mediated biochemical transformations. SAM is the sole methyl group donor involved in the methylation of DNA, RNA and histones, modulating the autophagic process by mediating epigenetic effects. Moreover, the metabolites of SAM, such as homocysteine, glutathione, decarboxylated SAM and spermidine, also exert important influences on the regulation of autophagy. From our perspective, nuclear‐cytosolic SAM is a conserved metabolic inhibitor that connects cellular metabolic status and the regulation of autophagy. In the future, SAM might be a new target of autophagy regulators and be widely used in the treatment of various diseases.

中文翻译:


S-腺苷甲硫氨酸:对自噬调节至关重要的代谢物



自噬是一种使细胞能够在饥饿条件下通过去除受损物质并调动能量储备来维持细胞稳态的机制。尽管营养物质的可用性强烈影响自噬过程,但调节自噬反应的具体代谢物尚未确定。最近的结果表明,S-腺苷甲硫氨酸(SAM)是甲硫氨酸饥饿诱导的自噬的关键抑制剂。 SAM 主要参与四个关键代谢途径:转甲基化、转硫作用、多胺合成和 5'-脱氧腺苷 5'-自由基介导的生化转化。 SAM 是参与 DNA、RNA 和组蛋白甲基化的唯一甲基供体,通过介导表观遗传效应来调节自噬过程。此外,SAM的代谢产物,如同型半胱氨酸、谷胱甘肽、脱羧SAM和亚精胺,也对自噬的调节产生重要影响。从我们的角度来看,核胞质 SAM 是一种保守的代谢抑制剂,将细胞代谢状态和自噬调节联系起来。未来,SAM可能成为自噬调节因子的新靶点,广泛应用于多种疾病的治疗。
更新日期:2020-10-08
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