Therapeutic applications of mesenchymal stem cell-derived extracellular vesicles in pain management: A narrative review of emerging evidence and future directions

Figure 1 Schematic representation of extracellular vesicle-mediated modulation of nuclear factor kappa B-light chain enhancer of activated B cells signaling pathway. Under inflammatory stimulation, receptor activation triggers the inhibitor of kappa B (IκB) kinase complex, leading to IκB phosphorylation and degradation, allowing nuclear factor kappa B to translocate into the nucleus and induce the expression of pro-inflammatory cytokines. Extracellular vesicle-derived microRNAs inhibit IκB kinase activity, thus stabilizing IκB and suppressing nuclear factor kappa B activation and downstream cytokine release. This mechanism helps reduce microglial activation and mitigate neuroinflammation. NF-кB: Nuclear factor kappa B; IκB: Inhibitor of kappa B; IKK: Inhibitor of kappa B kinase; EVs: Extracellular vesicles; TNF: Tumor necrosis factor; IL: Interleukin.