NOS2 and metabolic syndrome: The neuroinflammatory aMGCs enzymatic iNOS, NADPH Ox and Mt-derived excessive ROS due to aberrant mitochondria may interact and fuel other sources of ROS/NOS such as: Metabolic excess, hormonal excess, renin angiotensin aldosterone system activation, inflammation systemic or neuroinflammatory, hypoxia-ischemia, ischemia-reperfusion, eNOS uncoupling associated with EC dysfunction as in the MetS in Section 1.2 (Figure 2).