INTRODUCTION
Photoaging is the consequence of cumulative environmental exposure of human skin to light from across the electromagnetic (EM) spectrum. It is a complex, dynamic process that clinically manifests as cutaneous rhytides, atrophy, laxity, dyspigmentation, telangiectasias, roughness, and mottled appearance of the skin.1 Chronic solar radiation leads to cutaneous biologic effects including dermal damage and increased risk of skin cancers.2 Cycles of skin damage and imperfect repair create a compromised extracellular matrix (ECM).2 The mechanism of photoaging shares features with that of normal, chronologic aging, but it also has its own distinguishing features. Portions of the EM spectrum that are known to have cutaneous biologic effects include the ultraviolet (UV) (10 to 400 nm), visible light (VL) (400 to 700 nm), and infrared (IR) (700 nm to 1 mm) regions.3 UV-induced photoaging mechanisms are well established. Recent research has also examined the impact of light beyond the UV range. Early research shows that varied skin types may elicit different photobiologic responses to this range of light. This article presents the mechanisms and biomarkers of photodamage induced by light from across the spectrum, including UV, VL, and IR, to better prevent and reverse the damage of photoaging in all skin types.
UV-Induced Photodamage
There is an abundance of research establishing the mechanism of UV-induced photodamage as it is a significant source of photoaging and skin cancers. UV activates surface growth factors and cytokine receptors on keratinocytes and fibroblasts.2 Epidermal growth factor (EGF), IL-1, and TNF-alpha receptors activate within 15 minutes of UV exposure via phosphorylation of tyrosine kinase receptors (Figure 1).4 These protein kinase pathways lead to upregulated matrix metalloproteinases (MMPs), which are responsible for breaking down collagen.4 Through the MAPK pathway, UV also upregulates AP-1, a transcription factor that interferes with TGF-beta and collagen gene expression.5,6 UV induces reactive oxygen species (ROS) which additionally impairs TGF-beta causing damage in DNA, proteins, and lipids.2,6 Subsequent collagen fragmentation decreases tension on fibroblasts which further increases MMP expression and exacerbates cycles of collagen loss.1
Advanced glycation end products (AGEs) also contribute to photoaging.9 AGEs are photosensitizers of UVA radiation that lead to increased ROS.9 Accumulations of AGEs are found
UV can be further broken down into UVA (320 to 400 nm) and UVB (290 to 320 nm).3 UVA induces chromophores, the molecules that absorb incident photons of light, to generate ROS, resulting in DNA base modifications.7 Flavins, porphyrins, and bilirubin are the main chromophores for UVA.7 UVA penetrates more deeply into the dermis compared to UVB.8 DNA is the main chromophore for UVB.7 UVB directly induces cyclobutene pyrimidine dimers (CPDs).7 UVB is absorbed most by the epidermis and the DNA of keratinocytes.8
Advanced glycation end products (AGEs) also contribute to photoaging.9 AGEs are photosensitizers of UVA radiation that lead to increased ROS.9 Accumulations of AGEs are found
