Modulating poststroke inflammatory mechanisms: Novel aspects of mesenchymal stem cells, extracellular vesicles and microglia

Figure 1 Signaling pathways describing the process of polarization of the M2 phenotype. Damaged neurons induced by ischemic stroke activate resting microglia by producing damage-associated molecular pattern molecules. M1 phenotype microglia participate in the proinflammatory tissue response, whereas M2 microglia produce antiinflammatory substances. DAMPs: Damage-associated molecular pattern molecules; PPAR: Peroxisome proliferator-activated receptor; CREB: c-AMP response element binding protein; NF-κB: Nuclear factor-κB; YM1: Chitinase-3 Like protein; CD: Cluster of differentiation; STAT: Signal transducer and activator of transcription; ROS: Reactive oxygen species; Arg-1: Arginase-1; TNF: Tumor necrosis factor; iNOS: Inducible nitric oxide synthase; TLR: Toll-like receptor; IGF-1: Insulin-like growth factor-1; IL: Interleukin; IFN: Interferon; FIZZI: Found in inflammatory zone 1; TGF: Transforming growth factors; MAPK: Mitogen-activated protein kinase.