Numerous physiological and pathological roles have been attributed to the formation of mitochondrial reactive oxygen species (ROS). However, the individual contribution of different mitochondrial processes independently of bioenergetics remains elusive and clinical treatments unavailable. A notable exception to this complexity is found in the case of monoamine oxidases (MAOs). Unlike other ROS-producing enzymes, especially within mitochondria, MAOs possess a distinct combination of defined molecular structure, substrate specificity, and clinically accessible inhibitors. Another significant aspect of MAO activity is the simultaneous generation of hydrogen peroxide alongside highly reactive aldehydes and ammonia. These three products synergistically impair mitochondrial function at various levels, ultimately jeopardizing cellular metabolic integrity and viability. This pathological condition arises from exacerbated MAO activity, observed in many cardiovascular diseases, thus justifying the exploration of MAO inhibitors as effective cardioprotective strategy. In this context, we not only summarize the deleterious roles of MAOs in cardiac pathologies and the positive effects resulting from genetic or pharmacological MAO inhibition, but also discuss recent findings that expand our understanding on the role of MAO in gene expression and cardiac development.

许多生理和病理作用归因于线粒体活性氧（ROS）的形成。然而，独立于生物能学的不同线粒体过程的个体贡献仍然难以捉摸，并且临床治疗不可用。这种复杂性的一个显着例外是单胺氧化酶 (MAO)。与其他产生 ROS 的酶（尤其是线粒体内的酶）不同，MAO 具有明确的分子结构、底物特异性和临床上可用的抑制剂的独特组合。 MAO 活性的另一个重要方面是同时产生过氧化氢以及高活性醛和氨。这三种产品在不同水平上协同损害线粒体功能，最终危害细胞代谢完整性和活力。这种病理状况是由于在许多心血管疾病中观察到的 MAO 活性加剧而引起的，因此证明了探索 MAO 抑制剂作为有效的心脏保护策略的合理性。在此背景下，我们不仅总结了 MAO 在心脏病中的有害作用以及遗传或药理学 MAO 抑制所产生的积极作用，而且还讨论了最新的发现，这些发现扩大了我们对 MAO 在基因表达和心脏发育中的作用的理解。