Abstract
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.
Highlights
The Cellular Players of NeuroinflammationThe new century, together with technological innovations, brought new insight into the intrinsic communication between the central nervous system (CNS) and the innate immune response
Neuroinflammation has been shown to play a pivotal role in CNS disorders, being mainly responsible for the neuronal cell loss and the exacerbation of the pathology
Mitochondria have a prominent part in this process: they are responsible for inflammasome assembly and reactive oxygen species (ROS) production, and they enclose a large amount of damage-associated molecular patterns (DAMPs), accountable for sustaining the inflammatory process
Summary
The new century, together with technological innovations, brought new insight into the intrinsic communication between the central nervous system (CNS) and the innate immune response. The resident key players of the neuroimmune system are glial cells These CNS immune cells are classified as macroglia (oligodendrocytes and astrocytes) and microglia, they regulate several physiological processes required for neuronal survival and brain function. The neuroimmune response performed by activated glial cells has a dichotomous role in the CNS On one side, it induces the activation of repairing and regenerating mechanisms (i.e., remyelination), while on the other, the uncontrolled release of inflammatory mediators as proinflammatory cytokines, reactive oxygen species (ROS), and nitric oxide (NO) boost a chronic neuroinflammatory state, and is potentially dangerous for the neighboring cells. We are going to discuss the current therapies aimed to reduce neuroinflammation in the cited pathologies
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