Alcohol use disorder (AUD) is characterized by compulsive binge alcohol intake, leading to various health and social harms. Protein Kinase C epsilon (PKCε), a specific family of PKC isoenzyme, regulates binge alcohol intake, and potentiates alcohol-related cues. Alcohol via upstream kinases like the mammalian target to rapamycin complex 1 (mTORC1) or 2 (mTORC2), may affect the activities of PKCε or vice versa in AUD. mTORC2 phosphorylates PKCε at hydrophobic and turn motif, and was recently reported to be associated with alcohol-seeking behavior, suggesting the potential role of mTORC2-PKCε interactions in the pathophysiology of AUD. mTORC1 regulates translation of synaptic proteins involved in alcohol-induced plasticity. Hence, in this article, we aimed to review the molecular composition of mTORC1 and mTORC2, drugs targeting PKCε, mTORC1, and mTORC2 in AUD, upstream regulation of mTORC1 and mTORC2 in AUD and downstream cellular mechanisms of mTORCs in the pathogenesis of AUD.

酒精使用障碍（AUD）的特征是强迫性饮酒，导致各种健康和社会危害。蛋白激酶Cε（PKCε）是PKC同工酶的一个特定家族，调节暴饮酒的摄入，并增强与酒精有关的提示。酒精通过上游激酶（如哺乳动物对雷帕霉素复合物1（mTORC1）或2（mTORC2）的靶向）可能会影响AUD中的PKCε活性，反之亦然。mTORC2磷酸化PKCε的疏水和转向基序，最近有报道与寻醇行为有关，这表明mTORC2-PKCε相互作用在AUD的病理生理中具有潜在作用。mTORC1调节涉及酒精诱导的可塑性的突触蛋白的翻译。因此，在本文中，我们旨在回顾mTORC1和mTORC2，靶向PKCε，mTORC1的药物，