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©Author(s) (or their employer(s)) 2026.
World J Stem Cells. Feb 26, 2026; 18(2): 116184
Published online Feb 26, 2026. doi: 10.4252/wjsc.v18.i2.116184
Figure 5
Figure 5 Extracellular vesicle-mediated modulation of mitogen-activated protein kinase and ion channel signaling in peripheral sensitization. Activation of mitogen-activated protein kinase (p38 and extracellular signal regulated kinase) increases transient receptor potential and voltage-gated sodium channel activity, leading to greater nociceptor excitability and pain sensitization. Extracellular vesicle-derived proteins and microRNAs can suppress p38/extracellular signal regulated kinase activation, normalizing transient receptor potential V1 and voltage-gated sodium channel function. This mechanism reduces peripheral sensitization and neuroinflammatory pain responses. EVs: Extracellular vesicles; miRNAs: MicroRNAs; MAPKs: Mitogen-activated protein kinases; ERK: Extracellular signal regulated kinase; TRP: Transient receptor potential; VGSC: Voltage-gated sodium channel; TRPV1: Transient receptor potential V1; NaV: Voltage-gated sodium.


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