More than a programmed cell growth arrest, cellular senescence can be viewed as a general cellular stress response that leads to profound morphological and behavioral changes. In vivo, the appearance of senescent cells could be linked to the exposures to internal and external stresses. In particular, ageing of the skin is influenced by external factors, of which mainly UV radiation, leading to skin photoageing. In vitro, the main skin cell types, when exposed to UVB, enter in premature senescence. However, the molecular pathways involved in the UV-induced senescence remain partly unknown. Recently, the Unfolded Protein Response (UPR) has been identified as playing a major role in the morphological changes associated with senescence. The aim of our research is to determine whether the UPR pathway is activated following UVB exposures and is involved in the establishment of UVB-induced senescence in human dermal fibroblasts. Our first results show that the three branches of the UPR (PERK, ATF6α, IRE1α) are activated after UVB stress. Moreover, by blocking their activation with specific chemical inhibitors, we showed that the ATF6α branch is involved in the induction of several senescence biomarkers following UVB exposures including SA-βgal activity, morphological changes and persistent DNA damage. In the next part of our work we will determine if this pathway impacts the composition of the Senescence Associated Secretory Phenotype. Ultimately, these results will allow us to determine whether the UPR pathway represents an interesting target capable of reducing or delaying age-related skin alterations.