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. 2021 Dec 6;13:772036. doi: 10.3389/fnagi.2021.772036

FIGURE 1.

FIGURE 1

Schematic diagram illustrating the signaling pathways involved in oxidative stress in early brain injury. iNOS, inducible nitric oxide synthase; PHB2, prohibitin 2; NRF2, nuclear factor erythroid 2-related factor 2; HO-1, heme oxygenase-1; NF-κB, nuclear factor kappa-B; KEAP1, Kelch-like epichlorohydrin-associated protein 1; ARE, antioxidant response element; MFGE8, milk fat globule–EGF factor-8; TLR4, toll-like receptor 4; TNF-α, tumor necrosis factor-α; GPR18, G protein-coupled receptor 18; p38 MAPK, mitogen-activated protein kinase; FPR2, formyl peptide receptor 2; ASK1, apoptosis signal-regulating kinase 1; Drp1, dynamin-related protein 1; OX40L, OX40 cognate ligand-protein; GPR54, G protein-coupled receptor 54; ARRB2, β-arrestin 2; GSK3β, glycogen synthase kinase-3β; PI3K, phosphatidylinositol 3-kinase; TGR5, trans-membrane G protein-coupled receptor-5; PGC-1α, peroxisome proliferators-activated receptor-γ coactivator-1α; NLRP3, NLR family, pyrin domain containing 3.