**8. Mechanisms of production of skin photodamage**

In a previous section, we discussed the importance of the exposome and one of its factors, sun exposure, which is closely linked to the skin photoaging process [7]. This photodamage is favored by the presence of trans-urocanic acid, a by-product of the epidermal protein filaggrin that is present in the skin and acts as a chromophore for solar radiation photons [19].


How does ROS act in the skin aging process?

• Activating cell receptors for pro-inflammatory cytokines: interleukin-1 (IL-1β), IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α), among others.

### **Figure 5.**

*Scheme of the mechanisms of photodamage production on the skin mediated by ROS. Image is taken from Altobelli, G.G. et al. (2020) "Copper/zinc superoxide dismutase in human skin: Current knowledge," Frontiers in medicine, 7. Available from: https://www.frontiersin.org/articles/10.3389/fmed.2020.00183/full*

• Inducing the activation of protein transcription factor 1 (AP-1), which activates matrix metalloproteinase enzymes (MMPs) that degrade collagen type I and III, while blocking the synthesis of pro-collagen I and III by inhibiting transforming growth factor beta (TGF-β) receptor signaling.

MMPs are proteolytic enzymes that are responsible for remodeling the extracellular matrix and that together can degrade all its constituents [21]. UV radiation triggers the production of pro-inflammatory cytokines that favor the expression of MMP-1, MMP-3, MMP-9, and MMP-12, which, as we have seen, accelerate the degradation of collagen, and favor the accumulation of elastin, generating manifestations of some signs of photoaging such as hyperpigmentation, telangiectasias, coarse skin texture, deep wrinkles, and solar elastosis [20, 22]. As MMPs also promote angiogenesis as a result of this stimulation, they favor cancer cell growth and spread (**Figure 5**) [23].
