Ultraviolet radiation (UVR) elicits complex, context‑dependent responses in the skin that reflect the balance between environmental stress and adaptive homeostatic mechanisms. The aryl hydrocarbon receptor (AhR) occupies a central position in this interface, acting as a tunable environmental sensor that can mediate both photodamage and photoprotection depending on ligand type, timing and cellular context. In this editorial, we discuss recent findings demonstrating that melatonin pretreatment attenuates UVR-induced AhR expression and downstream inflammatory and photoaging‑associated responses in human skin ex vivo. We propose that these effects are best interpreted within a Yin-Yang framework of AhR signalling, in which transient, ligand‑specific activation initiates protective programmes followed by timely signal termination, rather than simple pathway inhibition. Melatonin and its metabolites may function as short‑lived AhR agonists that promote adaptive antioxidant and cytoprotective responses while preventing sustained, maladaptive activation. This conceptual refinement aligns with emerging insights into photo‑neuro‑immuno‑endocrine regulation of skin homeostasis and highlights AhR signalling as a flexible regulatory axis integrating ultraviolet exposure, endogenous metabolism and cutaneous defence mechanisms.
Slominski et al. (Fri,) studied this question.