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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: A review of the role of cav-1 in neuropathology and neural recovery after ischemic stroke

Fig. 5

Schematic representation illustrating the role of caveolin-1 in regulating BBB permeability, neuroinflammantion, free radicals, apoptosis, angiogenesis, and neurogenesis and showing some of the signaling pathways coupling caveolae/caveolins with IS. Changing BBB permeability via transcytosis, MMP, and TJ; regulating neuroinflammantion via TLR4, IL-1β, SVCT2, COX2, MKK/P38MAPK, MyD88/NF-ΚB, and eNOS-IRAK4-NFκB pathway; altering free radicals via reducing NOS and ROS; influencing apoptosis through intrinsic apoptotic pathway and extrinsic apoptotic pathway and protecting astrocytes from apoptosis via Ras/Raf/ERK pathway; promoting angiogenesis through cav-1/VEGF and cav-1/NO pathway; and promoting neurogenesis via cav-1/VEGF pathway and neuroplasticity through NMDAR, TrkB, ERK, and PKA pathway. Interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), mitogen-activated protein kinase (MAPK), reactive nitrogen species (RNS), reactive oxygen species (ROS), extracellular signal-regulated kinase (ERK), vascular endothelial growth factor (VEGF), N-methyl-D-aspartate receptor (NMDAR)

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