The mechanism of photoaging — how UVA and UVB affect skin

Have you heard the term "photoaging"? Unlike natural aging from chronological age, it refers to skin aging caused by the accumulation of UV exposure. Here, we explain how UVA and UVB each affect the skin and their mechanisms.

UVB effects — DNA damage in the epidermis

UVB (280-315nm) primarily acts on the epidermis. When absorbed by the DNA of epidermal cells, adjacent thymine bases form abnormal bonds, creating thymine dimers (CPDs). This is the direct cause of DNA damage.

When damage accumulates, cells either undergo apoptosis (cell death) or fail to repair correctly, resulting in mutations. These are known as "sunburn cells," and in the long term, they become a risk factor for skin cancer.

UVA effects — Collagen degradation in the dermis

UVA (315-400nm) has a longer wavelength than UVB and penetrates to the dermis, where it degrades collagen and elastin. Specifically, UVA acts on fibroblasts and upregulates the expression of matrix metalloproteinases (MMPs).

MMPs are enzymes that cleave collagen fibers. Chronic UVA exposure causes collagen degradation to exceed synthesis, leading to structural collapse of the dermis. This is what causes wrinkles and sagging.

Generation of reactive oxygen species (ROS)

Both UVA and UVB generate large amounts of reactive oxygen species (ROS) in the skin. ROS oxidize cell membrane lipids, denature proteins, and damage DNA. Vitamin C and Vitamin E and other antioxidant ingredients are valued precisely because they neutralize these ROS.

Photoaging vs natural aging

Photoaging and natural aging produce different changes in the skin. Natural aging is characterized by fine wrinkles and skin thinning. Photoaging, on the other hand, causes deep wrinkles, dark spots, and skin thickening (leathery changes).

Comparing areas rarely exposed to UV (inner arm, abdomen) with constantly exposed areas (face, back of hands) reveals a stark difference even at the same age. This contrast demonstrates the enormous impact of photoaging.