Exposure of human melanocytes to UVB twice and subsequent incubation leads to cellular senescence and senescence-associated pigmentation through the prolonged p53 expression

Skin aging is induced both intrinsically and extrinsically, with intrinsic aging reflecting the genetic background and dependent upon the passage of time, whereas extrinsic aging is caused by environmental factors, such as ultraviolet radiation (UVR), smoking, alcohol abuse, and poor nutrition [1,2]. Among these environmental factors, UVR contributes to up to 80% of the acceleration of skin aging by inducing DNA damage (photoaging) or by activation of diverse oncogenes [3]. To prevent DNA damage by UVR, skin cells harbor well-coordinated systems, including those associated with cell cycle checkpoints, DNA repair, apoptosis, and premature senescence.