Why Does the Sun Damage Our Skin?

Why Does the Sun Damage Our Skin?

Sunlight may be the source of life, but over time, it can become a destructive enemy for the skin. Intense sun exposure, especially during the summer months, is one of the main causes of skin aging, also known as photoaging. However, this process isn't limited to wrinkles. This change, which causes damage at the molecular level in the deep skin layers, occurs through a complex chain reaction ranging from cellular aging to enzymatic destruction.

So how do UV rays damage the skin? How do oxidative stress, enzymes, and genetic factors play a role in this process? In this article, we examine the cellular mechanisms that cause photoaging with scientific data.

What is Oxidative Stress and How Does It Damage the Skin?
When UV rays are absorbed by molecules such as melanin, urocanic acid, and NADH in the skin, reactive oxygen species (ROS) are released. These harmful molecules:

Oxidize DNA, protein, and lipid membranes, causing structural damage.

Stimulate growth factor receptors on the cell surface, triggering inflammatory signals.

The breakdown of membrane lipids increases ceramide release, leading to the activation of transcription factors such as AP-1.

This process ultimately leads to chronic damage, inflammation, and premature aging in cells.

UVA and UVB: Different Rays, Different Damages
UVA: Reaches deeper skin layers, triggering inflammation and ROS production. It disrupts cell metabolism, particularly through prostaglandins and lipid mediators.

UVB: Causes more superficial but direct DNA damage. It activates transcription factors such as NF-κB in keratinocytes and increases NADPH oxidase production, increasing ROS levels.

Both wavelengths accelerate cell aging in the skin through different mechanisms and contribute to a weakened immune system.

How Are Autophagy and Proteasomes Affected in Photoaging?
Autophagy, the self-cleaning and renewal mechanism of cells, plays a critical role in the photoaging process. UVA and UVB rays:

They stimulate autophagy in fibroblasts, but this mechanism becomes insufficient in the long term.

Proteasome activity decreases after UVB exposure, leading to the accumulation of intracellular waste and an aging phenotype.

In this case, cells either enter the premature aging process or are forced into apoptosis (programmed cell death).

Enzymatic Degradation: MMPs and Photoaging
UV rays increase the production of matrix metalloproteinases (MMP-1, MMP-3, MMP-9), enzymes that break down collagen, elastin, and other connective tissue proteins, the building blocks of skin. This leads to:

Decreased skin elasticity

Deepening wrinkles

Skin sagging.

Increased MMPs are directly related to ROS production. These enzymes may also play a role in cancer processes.

Cathepsins and New Biomarkers
Recent research indicates that levels of cathepsin B, D, K, and G enzymes change during photoaging. Specifically:

Catepsin K is the main enzyme that breaks down elastin fibers.

Catepsin D can suppress the immune system and affect keratinocyte growth.

Catepsin B increases cell invasion and tissue destruction.

The levels of these enzymes can be used as biomarkers in photoaging skin.

Opsin 3 (OPN3) and New Discoveries
Opsin 3 (OPN3), activated by UVA rays, is a novel signaling pathway that initiates MMP production in fibroblasts. This pathway:

Works through G proteins, protein kinase II, Ca2+/calmodulin, and other molecular signals.

This, in turn, triggers factors such as AP-1 and MAPK, initiating collagen degradation.

This finding may offer new therapeutic targets for the molecular control of photoaging.

AP-1 and NF-κB: Two Key Signature Factors of Photoaging
AP-1: Activated by ROS, it increases the transcription of MMPs and also suppresses TGF-β signaling, reducing collagen production.

NF-κB: Regulates the gene expression of cytokines and adhesion molecules and contributes to the photoaging process by increasing MMP-1 and MMP-3.

These two factors control both the structural and inflammatory aspects of skin aging.

Conclusion: What to Do About Photoaging?
Photoaging is not only an aesthetic problem; it is also a sign of profound damage at the cellular level and a weakened immune system. To slow or prevent this process:

Using broad-spectrum sunscreen (UVA + UVB protection)

Products containing antioxidants (vitamin C, vitamin E, niacinamide)

DNA-repairing cosmeceuticals

Skin-rejuvenating laser and medical treatments

Individual skin planning with expert dermatological follow-up

is important.

???? Don't leave your skin vulnerable to the harmful effects of the sun.
???? Follow the path of healthy skin, not aging, with our skin care and protection protocols prepared in light of scientific data at Ankara Life Polyclinic.
????‍⚕️ Dermatologist Dr. Fatma Yıldız