Figure 1.

Possible mechanisms of OS mediating in skin diseases. Exogenous insults (UV, IR, ischemia-hypoxia, etc.) and/or endogenous factors (oxidase, metabolism) induce ROS overproduction, far beyond of antioxidant defense capability triggering OS occurrence; OS, then, facilitates macromolecules damage (including DNA injury, LPO, protein oxidation) and mediates in several related signaling pathways (e.g. Nrf2, MAPKs, NF-κB, JAK-STAT, PI3K/Akt), eventually resulting in various dermatoses such as psoriasis, chloasma, vitiligo, skin photodamage, skin tumour, SSc, AD, pemphigus and so on.

Notes: ⊕indicates ‘activation’; ⊖indicates ‘inhibition or suppression’.