The summer season, characterized by increased exposure to solar radiation, poses a significant challenge to skin homeostasis. Enhanced ultraviolet (UV) radiation combined with elevated temperatures initiates a series of complex biochemical processes within the skin. These processes result not only in signs of premature skin aging (photoaging) but also pigmentary disorders and an increased risk of skin cancer development. Understanding the molecular mechanisms underlying photodamage is crucial for developing effective preventive and therapeutic strategies.
Types of UV Radiation and Mechanisms of Action
Ultraviolet radiation is classified into three types: UVA (320–400 nm), UVB (280–320 nm), and UVC (100–280 nm). UVC is almost completely absorbed by the ozone layer and does not reach the Earth’s surface. In contrast, UVB and UVA penetrate the atmosphere and exert differential effects on skin structure andfunction.
Figure 1. Types of UV radiation and their skin penetration. UVA penetrates deeper into the skin than UVB and UVC but does not cause significant damage to the epidermis. Conversely, UVB primarily affects the superficial skin layers, causing sunburn and significantly contributing to skin cancer development. Due to its short wavelength, UVC is almost entirely absorbed by the ozone layer and does not reach the Earth’s surface. (Nutraceuticals for Skin Care: A Comprehensive Review of Human Clinical Studies, E. Barrajón-Catalán and others, 2018)
UVA, constituting approximately 95% of total UV radiation, is characterized by its deep penetration reaching the dermis. Its primary mechanisms of action include:
- Generation of Reactive Oxygen Species (ROS): UVA indirectly damages the dermis by inducing oxidative stress. ROS lead to lipid peroxidation of cell membranes, oxidation of proteins (including key enzymes and structural proteins), and damage to mitochondrial and nuclear DNA;
- Activation of Matrix Metalloproteinases (MMPs): UVA stimulates the expression and activity of MMPs (notably MMP-1, collagenase). These enzymes degrade key extracellular matrix (ECM) components such as type I and III collagen and elastin, resulting in loss of skin structural integrity, thinning, and wrinkle formation.
In contrast, UVB, despite having higher energy, penetrates the skin more superficially and mainly affects the epidermis, causing:
- Direct DNA damage: UVB is directly absorbed by nucleic acids, leading to the formation of DNA photoproducts. Unrepaired DNA damage may result in mutations, apoptosis (forming characteristic sunburn cells), or, in worst cases, oncogenic transformation;
- Induction of melanogenesis: UVB strongly stimulates melanocytes to produce excessive melanin by activating cellular signaling pathways that increase tyrosinase activity, a key enzyme in melanin synthesis. While melanin provides photoprotection, its overproduction and uneven distribution lead to hyperpigmentation (melasma, age spots, freckles);
- Induction of inflammation: UVB triggers a robust inflammatory response via release of proinflammatory cytokines, causing erythema and structural skin damage.
Photoaging, a complex and chronic process of structural and functional skin changes, is induced by prolonged UV exposure. The effects of UV radiation, including ECM degradation (notably solar elastosis) and pigmentation disorders, result from intricate alterations in keratinocytes, melanocytes, and fibroblasts. Particularly, morphological changes in fibroblasts play a key role in collagen degradation, which is a primary cause of wrinkle formation and loss of skin firmness.
Preventive Skin Fortification: The Role of Native Hyaluronic Acid
Skin exposed to intense UV radiation requires appropriate preconditioning aimed at enhancing its intrinsic defense mechanisms. One of the most effective approaches in this context is biostimulation via intradermal injections of native, non-crosslinked hyaluronic acid (HA). This method constitutes a proactive strategy for reinforcing and regenerating the skin’s structure and function.
Native hyaluronic acid is a naturally occurring polysaccharide and a fundamental component of the extracellular matrix. Its role in maintaining tissue homeostasis involves intensive hydration, structural integrity support, and modulation of key physiological processes. HA acts as a potent biostimulatory and hydrating agent, and its mechanisms of action encompass the following:
- Restoration of optimal tissue hydration: HA exhibits pronounced hygroscopic properties, allowing it to bind water up to 1,000 times its own molecular weight within the extracellular matrix. These hydrophilic characteristics are crucial for maintaining adequate tissue hydration, osmotic balance, and, consequently, improving skin elasticity and barrier function
- Fibroblast stimulation: HA interacts with cell surface receptors on fibroblasts, particularly CD44, thereby promoting their proliferation and enhancing the synthesis of endogenous HA, collagen, and elastin. This activity leads to the remodeling and densification of the dermal matrix. The HA-induced upregulation of ECM proteins is pivotal in restoring dermal firmness and elasticity, counteracting degenerative changes associated with photoaging;
- Antioxidant activity: HA demonstrates the capacity to scavenge ROS, thereby protecting cells from UV-induced oxidative stress. This mechanism involves both direct neutralization of free radicals and indirect modulation of intracellular signaling pathways associated with oxidative stress responses. As a result, HA mitigates lipid peroxidation, DNA damage, and protein denaturation, thus preserving cellular homeostasis and viability.
Preventive application of a series of treatments with native, non-crosslinked hyaluronic acid is an effective method to prepare the skin for intensive UV exposure during the summer. Such biostimulation effectively supports endogenous skin regenerative and defensive mechanisms, significantly improving baseline skin condition and increasing resistance to photodamage. Consequently, there is an enhanced capacity of the skin to neutralize oxidative stress and limit cumulative damage caused by UV radiation.
Achieving effective photoaging prevention, however, requires a holistic and integrated approach. This encompasses not only the aforementioned biostimulatory treatments but also consistent photoprotection and implementation of advanced, personalized skincare. Individualized protective strategies tailored to skin phototype, current condition, and specific environmental factors are essential. This approach enables optimal therapeutic outcomes, maintaining healthy, resilient, and radiant skin resistant to the long-term effects of UV exposure.