biomolecules Review The Dichotomous Role of Inflammation in the CNS: A Mitochondrial Point of View Bianca Vezzani 1,2 , Marianna Carinci 1,2 , Simone Patergnani 1,2 , Matteo P. Pasquin 1,2, Annunziata Guarino 2,3, Nimra Aziz 2,3, Paolo Pinton 1,2,4, Michele Simonato 2,3,5 and Carlotta Giorgi 1,2,* 1 Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy;
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[email protected] (P.P.) 2 Laboratory of Technologies for Advanced Therapy (LTTA), Technopole of Ferrara, 44121 Ferrara, Italy;
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[email protected] (M.S.) 3 Department of BioMedical and Specialist Surgical Sciences, University of Ferrara, 44121 Ferrara, Italy 4 Maria Cecilia Hospital, GVM Care & Research, 48033 Cotignola (RA), Italy 5 School of Medicine, University Vita-Salute San Raffaele, 20132 Milan, Italy * Correspondence:
[email protected]; Tel.: +39-0532-455803 Received: 28 August 2020; Accepted: 10 October 2020; Published: 13 October 2020 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.