The role of mitochondria spans from the regulation of the oxidative phosphorylation, cell metabolism and survival/death pathways to a more recently identified function in chronic inflammation. In stress situations, mitochondria release some pro-inflammatory mediators such as ATP, cardiolipin, reactive oxygen species (ROS) or mitochondrial DNA, that are believed to participate in chronic diseases and aging. These mitochondrial Damage-Associated Molecular Patterns (mito-DAMPs) can modulate specific receptors among which TLR9, NLRP3 and cGAS-STING, triggering immune cells activation and sterile inflammation. In order to counter the development of chronic diseases, a better understanding of the underlying mechanisms of low grade inflammation induced by mito-DAMPs is needed. In this context, monoamine oxidases (MAO), the mitochondrial enzymes that degrade catecholamines and serotonin, have recently emerged as potent regulators of chronic inflammation in obesity-related disorders, cardiac diseases, cancer, rheumatoid arthritis and pulmonary diseases. The role of these enzymes in inflammation embraces their action in both immune and non-immune cells, where they regulate monoamines levels and generate toxic ROS and aldehydes, as by-products of enzymatic reaction. Here, we discuss the more recent advances on the role and mechanisms of action of MAOs in chronic inflammatory diseases.

中文翻译：

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单胺氧化酶：慢性病中线粒体和炎症之间缺失的环节 ？


线粒体的作用从调节氧化磷酸化、细胞代谢和生存/死亡途径到最近确定的慢性炎症功能。在压力情况下，线粒体会释放一些促炎介质，如 ATP、心磷脂、活性氧 （ROS） 或线粒体 DNA，这些介质被认为与慢性疾病和衰老有关。这些线粒体损伤相关分子模式 （mito-DAMPs） 可以调节特定受体，其中包括 TLR9、NLRP3 和 cGAS-STING，触发免疫细胞活化和无菌炎症。为了对抗慢性病的发展，需要更好地了解 mito-DAMPs 诱导的低度炎症的潜在机制。在此背景下，单胺氧化酶 （毛），即降解儿茶酚胺和血清素的线粒体酶，最近已成为肥胖相关疾病、心脏病、癌症、类风湿性关节炎和肺部疾病中慢性炎症的有效调节剂。这些酶在炎症中的作用包括它们在免疫和非免疫细胞中的作用，它们调节单胺水平并产生有毒的 ROS 和醛，作为酶反应的副产物。在这里，我们讨论了 MAO 在慢性炎症性疾病中的作用和作用机制的最新进展。