Mechanisms and Care for Anti-Aging Skin

The anti-aging effects of cosmetics are an eternal topic. Generally, they work by long-term repair of the extracellular matrix to make the skin firm, or by adding antioxidants to reduce free radical damage to the skin, regulate immunity, and enhance the skin’s self-protection. They may also include plant oils to improve skin aging, accelerate protein secretion, and prevent skin aging. Natural active antioxidants can effectively prevent pigmentation caused by UV rays and other harmful radiation, thereby improving skin radiance.

Mechanisms of Skin Aging

Skin aging is mainly divided into natural aging and photoaging. Natural aging is caused by internal factors of the body and is common in both exposed and non-exposed areas, characterized by the appearance of wrinkles and skin sagging. Photoaging refers to the accumulation of UV damage during the skin aging process, manifested as rough skin, deepened and thickened wrinkles, abnormal structure, pigmentation, vascular dilation, and epidermal keratosis in exposed areas.

Skin aging results from the combined effects of endogenous (natural aging) and exogenous factors. Endogenous factors are mainly formed by the combined effects of genetic genes and free radical damage to cells. The endogenous mechanisms of skin aging are very complex, and no single theory can fully explain the phenomenon of aging. More comprehensive aging theories include genetic theory, free radical theory, neuroendocrine function decline theory, and Others. Exogenous factors mainly include photoaging caused by solar radiation, as well as the hazards of chemicals and poor lifestyle habits.

Exogenous factors play an important role in skin aging, not only accelerating the normal physiological aging process of the skin but also having their own characteristics. For example, long-term exposure to UV rays is the most common and strongest external factor causing skin aging. Cigarette smoke is also a significant exogenous factor; smoking can promote skin aging, and its effect on skin aging is comparable to that of UV rays, with both having a synergistic effect. Cigarettes are the largest source of free radicals, and oxidative damage caused by free radicals is an important factor in skin aging and aging-related diseases.

Poor lifestyle habits can accelerate skin aging, such as long-term staying up late, frequent worry or irritability, improper rapid weight loss or lack of physical exercise, use of inferior cosmetics, excessive drinking, and consumption of strong tea and coffee. These habits can easily irritate the skin, reduce the ability of skin cells to divide and renew, and make the skin slack, thereby promoting skin aging. Skin aging and its manifestations vary greatly among individuals, and there is no biological rule to measure its intensity. It is evident that around the age of 50, during menopause, aging accelerates suddenly, a phenomenon known as hormone-induced skin aging. Hormone-induced skin aging is a significant event in a woman’s life, mostly occurring 4-5 years before the onset of menopause, known as the pre-menopausal period, emphasizing the period during menopause. Different individuals may show differences in certain physiological phenomena before and during menopause, which is an unavoidable aging brought by age, or more accurately, aging caused by hormonal imbalance.

Physiological aging is an extremely complex and inevitable internal process. Some reactions occurring during the aging process include free radical damage, collagen destruction, slowed cell metabolism, reduced abnormal cell shape and fat content, decreased intercellular substance, natural cell death, hormonal imbalance, and hypoxia. As a result, the skin shows changes such as wrinkles, age spots, and loss of elasticity.

Formation of Wrinkles

The mechanisms of wrinkle formation mainly include:

1. Dysfunction of the Stratum Corneum: This is primarily the cause of superficial wrinkles. Low moisture content in the stratum corneum and the resulting thickening of the stratum corneum lead to loss of skin softness and the formation of wrinkles.
2. Degradation of the Epidermis: As we age, the proliferative activity of epidermal cells declines, causing the epidermis to thin. Aging also leads to the flattening of the junction between the epidermis and dermis, resulting in loss of skin elasticity and wrinkle formation.
3. Reduction and Disorganization of Dermal Collagen Fibers: The decrease in collagen fibers, disorganization of collagen fiber bundles, and activation or increase of matrix metalloproteases (MMPs) due to UV exposure lead to the breakdown and fragmentation of collagen, causing loss of skin elasticity and wrinkle formation.
4. Elastin Degeneration: Prolonged UV exposure activates elastase, causing the breakdown and loss of elastic fibers (fine elastic fibers distributed vertically under the epidermis) or degeneration and bending of dermal elastin, leading to reduced skin elasticity and wrinkle formation.
5. Reduction of Hyaluronic Acid: With age, the amount of hyaluronic acid in the skin decreases, particularly reducing the water retention capacity of the epidermis, leading to wrinkle formation.
6. Damage to the Basement Membrane: The basement membrane, which is the junction between the epidermis and dermis, is composed of type IV collagen, laminin, and proteoglycans, providing mechanical strength to the skin. Long-term UV exposure induces the production of gelatinases (MMP-2 and MMP-9) in basal cells of the epidermis, damaging the basement membrane and leading to reduced skin elasticity and wrinkle formation.
7. Activation of Epidermal Heparanase: Heparan sulfate in the basement membrane binds with growth factors to restore their function. UV exposure increases epidermal heparanase activity, significantly degrading heparan sulfate, disrupting the regulation of growth factors controlled by heparan sulfate, causing damage to the epidermis, dermis, blood vessels, and lymphatic vessels, and promoting the formation of wrinkles and other photoaging phenomena.
8. Angiogenesis: UV exposure disrupts the balance of thrombospondin and vascular endothelial growth factors in the epidermis, inducing angiogenesis. Subsequently, elastase and MMP-producing neutrophils infiltrate the skin tissue, causing the breakdown and degeneration of elastin and collagen, leading to wrinkle formation.
9. Reduced Lymphatic Function: UV exposure decreases the lymphatic activator VEGF-C, slowing the recovery of macrophages, which remain in the dermis. This promotes the breakdown of elastin by MMP-12 (macrophage elastase) in macrophages, leading to wrinkle formation.
10. Generation of Reactive Oxygen Species (ROS) and Free Radicals: UV exposure generates free radicals and ROS in the skin, causing lipid peroxidation of cell membranes, protein denaturation due to the association of collagen and elastin fibers, inactivation of ROS-scavenging enzymes, DNA damage, and activation of MMP-1, 3, and 9, leading to dermal structural degeneration, reduced cell function, and wrinkle formation.