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UVR-induced DNA damage and alterations in the extracellular matrix (ECM) disrupt homeostasis and trigger cellular stress, leading to the activation of inflammatory responses in the skin as shown in Figure 2

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We hypothesized that this lipophilic feature could facilitate non-covalent incorporation of TZP into the hydrophobic domains of the PNP hydrogel network during formulation, without requiring chemical modification ( Figure 1D )

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This raises the possibility that GLP-1 medicines may reduce neuroinflammation both directly, through actions on neurons, and indirectly, by lowering systemic inflammation that contributes to neuroinflammatory processes