Photoaging: Pathogenesis, prevention, and treatment

UV irradiation of human skin sets in motion a complex yet traceable sequence of events that causes damage to the dermal matrix. Mapping of these pathways with measurements made from human skin in vivo has served to construct a framework of our understanding of photoaging pathophysiology. In the authors' model, the creation of invisible solar scars that accumulate with each subsequent exposure to UV irradiation, eventually leading to the visible solar scarring that we call photoaging, remains speculation. Mapping of the UV signaling cascade that leads to MMP induction has identified several potential targets for photoaging prevention strategies. Topical tretinoin, which is known to repair photodamage, also blocks UV induction of cJun, a key component of transcription factor AP-1 that is required for MMP expression. When topical tretinoin is applied to human skin, no distinction is made as to whether it is intended for treatment or for prevention of photoaging. Any collagen deficiency that exists in photoaged skin will be remedied. At the same time, tretinoin primes the skin to prevent UV induction of cJun, thereby blocking MMP induction. Thus, the use of topical tretinoin is central for the treatment and prevention of photoaging. Early work with antioxidants indicates that targeting ROS is likely to be another successful photoaging prevention strategy. Serious consideration also should be given to inhibitors of MMPs, MAP kinases, and even more proximal factors in the UV response. Clinicians' ability to treat and prevent photoaging will only improve when the approach is based on solid scientific evidence.