Fig. 4.

Putative mechanisms of inflammation-induced impairment of neurogenesis. During inflammation activated microglia produce pro-inflammatory cytokines, ROS and nitric oxide (NO), all of which inhibit mitochondrial function in neuronal progenitor cells (NPC). Mitochondrial damage leads to increased levels of mitochondrial ROS production and may suppress neurogenesis through mechanisms including Sirt1 oxidation. Severe impairment of mitochondrial function leads to cell death by necrosis or by activation of apoptotic signaling and activation of caspases. Other mechanisms connecting NPC mitochondrial function and neurogenesis require further investigation.