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An overview of cytokine factors related signaling pathways that are involved in TBI. I. Injured neurons release damage-associated molecular patterns (DAMPs) and HMGB1, which bind to TLR4. This activates microglia to produce more inflammatory factors and <t>Galectin-3.</t> At the same time, it initiates a cascade reaction with MyD88, promoting the entry of NF-κB into the nucleus to bind to the promoter and up-regulate the expression of NLPR3 and GMF. This accelerates the release of IL-1β and IL-18. Galectin-3 can also initiate an inflammatory response by binding to the TLR4 receptor. II. The binding of ligands (growth factors and cytokines) to specific receptors triggers a cascade reaction of MAPKs. These are activated by phosphorylation and ultimately induce microglia activation, oxidative stress, and blood-brain barrier damage. III. TGFβ1 binds to the receptor and initiates Smads protein phosphorylation. This inhibits microglia activation and protects the nerves, preventing myelin shedding. IV. After TBI, epidermal growth factor and insulin growth factor bind to tyrosine kinase receptors, initiating a cascade reaction that activates Akt. Akt participates in apoptosis by regulating the phosphorylation of the pro-apoptotic mediator GSK-3β.
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An overview of cytokine factors related signaling pathways that are involved in TBI. I. Injured neurons release damage-associated molecular patterns (DAMPs) and HMGB1, which bind to TLR4. This activates microglia to produce more inflammatory factors and <t>Galectin-3.</t> At the same time, it initiates a cascade reaction with MyD88, promoting the entry of NF-κB into the nucleus to bind to the promoter and up-regulate the expression of NLPR3 and GMF. This accelerates the release of IL-1β and IL-18. Galectin-3 can also initiate an inflammatory response by binding to the TLR4 receptor. II. The binding of ligands (growth factors and cytokines) to specific receptors triggers a cascade reaction of MAPKs. These are activated by phosphorylation and ultimately induce microglia activation, oxidative stress, and blood-brain barrier damage. III. TGFβ1 binds to the receptor and initiates Smads protein phosphorylation. This inhibits microglia activation and protects the nerves, preventing myelin shedding. IV. After TBI, epidermal growth factor and insulin growth factor bind to tyrosine kinase receptors, initiating a cascade reaction that activates Akt. Akt participates in apoptosis by regulating the phosphorylation of the pro-apoptotic mediator GSK-3β.
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An overview of cytokine factors related signaling pathways that are involved in TBI. I. Injured neurons release damage-associated molecular patterns (DAMPs) and HMGB1, which bind to TLR4. This activates microglia to produce more inflammatory factors and Galectin-3. At the same time, it initiates a cascade reaction with MyD88, promoting the entry of NF-κB into the nucleus to bind to the promoter and up-regulate the expression of NLPR3 and GMF. This accelerates the release of IL-1β and IL-18. Galectin-3 can also initiate an inflammatory response by binding to the TLR4 receptor. II. The binding of ligands (growth factors and cytokines) to specific receptors triggers a cascade reaction of MAPKs. These are activated by phosphorylation and ultimately induce microglia activation, oxidative stress, and blood-brain barrier damage. III. TGFβ1 binds to the receptor and initiates Smads protein phosphorylation. This inhibits microglia activation and protects the nerves, preventing myelin shedding. IV. After TBI, epidermal growth factor and insulin growth factor bind to tyrosine kinase receptors, initiating a cascade reaction that activates Akt. Akt participates in apoptosis by regulating the phosphorylation of the pro-apoptotic mediator GSK-3β.

Journal: Frontiers in Immunology

Article Title: Cytokines and related signaling pathways in traumatic brain injury

doi: 10.3389/fimmu.2026.1738589

Figure Lengend Snippet: An overview of cytokine factors related signaling pathways that are involved in TBI. I. Injured neurons release damage-associated molecular patterns (DAMPs) and HMGB1, which bind to TLR4. This activates microglia to produce more inflammatory factors and Galectin-3. At the same time, it initiates a cascade reaction with MyD88, promoting the entry of NF-κB into the nucleus to bind to the promoter and up-regulate the expression of NLPR3 and GMF. This accelerates the release of IL-1β and IL-18. Galectin-3 can also initiate an inflammatory response by binding to the TLR4 receptor. II. The binding of ligands (growth factors and cytokines) to specific receptors triggers a cascade reaction of MAPKs. These are activated by phosphorylation and ultimately induce microglia activation, oxidative stress, and blood-brain barrier damage. III. TGFβ1 binds to the receptor and initiates Smads protein phosphorylation. This inhibits microglia activation and protects the nerves, preventing myelin shedding. IV. After TBI, epidermal growth factor and insulin growth factor bind to tyrosine kinase receptors, initiating a cascade reaction that activates Akt. Akt participates in apoptosis by regulating the phosphorylation of the pro-apoptotic mediator GSK-3β.

Article Snippet: Clinically, plasma Galectin-3 levels correlate positively with Glasgow Coma Scale scores (r = 0.72, p < 0.001), underscoring its potential as a prognostic biomarker for TBI severity ( ).

Techniques: Protein-Protein interactions, Expressing, Binding Assay, Phospho-proteomics, Activation Assay