Inflammatory Molecules Associated with Ultraviolet Radiation-Mediated Skin Aging

Abstract

Skin is the largest and most complex organ in the human body comprised of multiple layers with different types of cells. Different kinds of environmental stressors, for example, ultraviolet radiation (UVR), temperature, air pollutants, smoking, and diet, accelerate skin aging by stimulating inflammatory molecules. Skin aging caused by UVR is characterized by loss of elasticity, fine lines, wrinkles, reduced epidermal and dermal components, increased epidermal permeability, delayed wound healing, and approximately 90% of skin aging. These external factors can cause aging through reactive oxygen species (ROS)-mediated inflammation, as well as aged skin is a source of circulatory inflammatory molecules which accelerate skin aging and cause aging-related diseases. This review article focuses on the inflammatory pathways associated with UVR-mediated skin aging.

Keywords: inflammation; skin aging; ultraviolet radiation (UVR).

Figure 1

Penetration of the solar ultraviolet radiation (UVR) into the skin. According to the wavelength, the UVR is classified into three categories: UVA, UVB, and UVC. UVC is blocked by the ozone layer, UVB can penetrate into the epidermis, and UVA can penetrate up to the dermis.

Figure 2

Inhibition of NF-κB-induced inflammation by klotho and SIRT1. NF-κB can be activated by different environmental stimuli as well as endogenous cytokines, such as TNF-α and IL-1. Klotho can inhibit the NF-κB pathway by preventing translocation of NF-κB or inhibiting TLR4-mediated NF-κB activation. SIRT1 prevents the NF-κB pathway by directly inhibiting NF-κB deacetylating NF-κB subunit. NF-κB, nuclear factor kappa light chain enhancer of activated B; TNF-α, Tumor necrosis factor; IL-1, Interleukin 1; TLR4, Toll-like receptor 4, SIRT1, Sirtuin 1.

Figure 3

Histological comparison between young and aged photo-exposed human skin. Skin specimens from (A) young: 12 years, and (B) aged: 77 years, are stained with hemotoxylin and eosin (HE) staining. Aged human skin epidermis is thinner compared to the young skin, as well as the aged dermis displays increased amounts of degenerated elastic fibers.

Figure 4

UVR-induced collagen degradation through the TGF-β pathway. UV radiation can cause a reduction in TGF-β type 2 receptor expression by producing ROS. It can also inhibit Smad2/Smad3 phosphorylation and nuclear translocation, resulting in decreasing Type 1 collagen expression and collagen degradation. UV, Ultraviolet; TGF-β, transforming growth factor; ROS, reactive oxygen species.

Figure 5

Major signaling pathways involved in UV-mediated photoaging. UV radiation can cause direct damage to the DNA, produce ROS, and disrupt skin barrier function. These can further activate many inflammatory receptors, which can lead to photoaging through inflammation and collagen degradation. UV, Ultraviolet; ROS, reactive oxygen species.