Alcohol exposure and stressful events in life can induce long-lasting changes in physiology, behavior and gene expression patterns, eventually facilitating the development of psychiatric diseases like alcohol use disorders (AUD). Epigenetic mechanisms have been recently proposed to play a role in the cellular actions of alcohol via chromatin remodeling. Here we discuss interactions between stress and the pharmacological effects of alcohol, including the possibility that early exposure to, or withdrawal of, alcohol might induce stressful effects of their own. A specific aim is to describe novel molecular mechanisms by which stress, alcohol or their combined presentation impact on the epigenome. A key question is why only a fraction of the population progresses from regular, non-problematic, alcohol use to AUD, despite suffering from similar alcohol exposure. It is important to analyze how environmental factors, most notably stress, interact with the epigenetic machinery to increase vulnerability for AUD. The knowledge derived from this endeavor will be critical for the development of preventive strategies and new, drug- or gene-based, therapies.

中文翻译：

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环境压力和酒精中毒的发展：关注分子靶标及其表观遗传调控。

酒中暴露和生活中的压力事件可引起生理，行为和基因表达模式的长期变化，最终促进诸如吸毒症（AUD）等精神疾病的发展。最近提出表观遗传机制通过染色质重塑在酒精的细胞作用中发挥作用。在这里，我们讨论了压力与酒精的药理作用之间的相互作用，包括及早暴露或戒除酒精可能会诱发其自身的压力作用的可能性。一个特定的目标是描述压力，酒精或它们的组合呈递对表观基因组产生影响的新分子机制。一个关键问题是，为什么只有一小部分人口从正常，无问题的饮酒发展为澳元，尽管遭受了相似的酒精暴露。重要的是分析环境因素（尤其是压力）如何与表观遗传机制相互作用，从而增加澳元的脆弱性。从这项工作中获得的知识对于制定预防策略和基于药物或基因的新疗法至关重要。