Innate immune response is one of our primary defenses against pathogens infection, although, if dysregulated, it represents the leading cause of chronic tissue inflammation. This dualism is even more present in the central nervous system, where neuroinflammation is both important for the activation of reparatory mechanisms and, at the same time, leads to the release of detrimental factors that induce neurons loss. Key players in modulating the neuroinflammatory response are mitochondria. Indeed, they are responsible for a variety of cell mechanisms that control tissue homeostasis, such as autophagy, apoptosis, energy production, and also inflammation. Accordingly, it is widely recognized that mitochondria exert a pivotal role in the development of neurodegenerative diseases, such as multiple sclerosis, Parkinson’s and Alzheimer’s diseases, as well as in acute brain damage, such in ischemic stroke and epileptic seizures. In this review, we will describe the role of mitochondria molecular signaling in regulating neuroinflammation in central nervous system (CNS) diseases, by focusing on pattern recognition receptors (PRRs) signaling, reactive oxygen species (ROS) production, and mitophagy, giving a hint on the possible therapeutic approaches targeting mitochondrial pathways involved in inflammation.

中文翻译：

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炎症在中枢神经系统中的二分作用：线粒体观点

先天免疫反应是我们抵御病原体感染的主要防御措施之一，尽管如果失调，它代表了慢性组织炎症的主要原因。这种二元论在中枢神经系统中更加存在，其中神经炎症对于激活修复机制很重要，同时导致释放导致神经元丢失的有害因素。调节神经炎症反应的关键因素是线粒体。事实上，它们负责控制组织稳态的各种细胞机制，例如自噬、细胞凋亡、能量产生以及炎症。因此，人们普遍认为线粒体在神经退行性疾病的发展中发挥着关键作用，例如多发性硬化症、帕金森病和阿尔茨海默病，以及急性脑损伤，如缺血性中风和癫痫发作。在这篇综述中，我们将通过关注模式识别受体 (PRR) 信号、活性氧 (ROS) 产生和线粒体自噬来描述线粒体分子信号在调节中枢神经系统 (CNS) 疾病中神经炎症中的作用，并给出提示关于靶向参与炎症的线粒体途径的可能治疗方法。