How your skin ages

The skin, as the largest human organ exposed to the external environment, suffers from both external and internal factors of aging. Skin aging is characterized by processes such as the formation of wrinkles, loss of elasticity and a rough appearance. This aging process is associated with phenotypic changes in the cells as well as changes in the matrix (structures such as collagens and elastin). This review will summarize the changes that occur during skin aging, advances in research into the molecular mechanisms causing these changes, and treatment strategies to prevent or reverse skin aging.

The skin is a barrier that separates the body from the external environment. In addition to protection against water loss and infections, it has an important cosmetic role. Young and beautiful looking skin can affect your mood and reproductive status. However, organ aging since our birth is no exception to the skin, as the largest human organ by volume, the skin shows obvious and visible signs of aging with age. Thus, many people, especially women, spend large amounts of time and money on cosmetic treatments and pharmaceuticals that can prevent or reverse skin aging. Wide cosmetic demand promotes research on skin aging. Skin aging is induced by both intrinsic and extrinsic factors. Intrinsic aging is caused by inevitable physiological processes, which cause progressive atrophy and the formation of wrinkles. External factors, on the other hand, are related to processes and phenomena such as air pollution, smoking, malnutrition and sun exposure. In particular, exposure to ultraviolet (UV) radiation is a major external factor in skin aging, also known as photoaging. This assessment will summarize the changes that occur as the skin ages, research advances in understanding the molecular mechanisms that cause these changes, and treatment strategies. Exposure to ultraviolet (UV) radiation is the primary external factor in skin aging, also known as photoaging. This assessment will summarize the changes that occur as the skin ages, research advances in understanding the molecular mechanisms that cause these changes, and treatment strategies. Exposure to ultraviolet (UV) radiation is the primary external factor in skin aging, also known as photoaging. This assessment will summarize the changes that occur as the skin ages, research advances in understanding the molecular mechanisms that cause these changes, and treatment strategies.

Changes during the internal aging of the skin.

Intrinsic skin aging is a chronologically progressive physiological change. Aging in areas protected from the sun is mainly related to genetic and metabolic factors, and in unprotected areas it is mainly related to external factors, especially UV radiation. For intrinsically aging skin, the most important histological changes occur in the basal cell layer. Studies have shown that cell proliferation in this layer decreases with ageing. The epidermis becomes thinner and the contact surface between the dermis and the epidermis decreases, resulting in poorer nutrient exchange and further weakening of proliferation. This process of reduced ability of cells to proliferate, including keratinocytes, fibroblasts and melanocytes is known as cellular senescence (cellular senescence). In skin samples from human donors of various ages, it has been shown that the expression of the marker beta-galactosidase in dermal fibroblasts is age-dependent, indicating that senescence is stronger in old skin. Additionally, old skin protected from light shows less mast cells, fibroblasts, collagen and elastin than young skin. There are studies suggesting that the production of procollagen 1 in intrinsically aged skin is likely reduced by regulation of TGF-beta/Smad signals and related tissue growth factors, which are believed to be regulators of collagen expression. In addition, there is evidence that aged skin internally has degenerated oligasaccharides, which makes it less able to bind water. this indicates that senescence is stronger in old skin. Additionally, old skin protected from light shows less mast cells, fibroblasts, collagen and elastin than young skin. There are studies suggesting that the production of procollagen 1 in intrinsically aged skin is likely reduced by regulation of TGF-beta/Smad signals and related tissue growth factors, which are believed to be regulators of collagen expression. In addition, there is evidence that aged skin internally has degenerated oligasaccharides, which makes it less able to bind water. this indicates that senescence is stronger in old skin. Additionally, old skin protected from light shows less mast cells, fibroblasts, collagen and elastin than young skin. There are studies suggesting that the production of procollagen 1 in intrinsically aged skin is likely reduced by regulation of TGF-beta/Smad signals and related tissue growth factors, which are believed to be regulators of collagen expression. In addition, there is evidence that aged skin internally has degenerated oligasaccharides, which makes it less able to bind water. that the production of procollagen 1 in intrinsically aged skin is likely reduced by regulation of TGF-beta/Smad signals and related tissue growth factors, which are believed to be regulators of collagen expression. In addition, there is evidence that aged skin internally has degenerated oligasaccharides, which makes it less able to bind water. that the production of procollagen 1 in intrinsically aged skin is likely reduced by regulation of TGF-beta/Smad signals and related tissue growth factors, which are believed to be regulators of collagen expression. In addition, there is evidence that aged skin internally has degenerated oligasaccharides, which makes it less able to bind water.

Changes during external aging of the skin.

As early as 1969, it was proposed that, in addition to intrinsic factors, exposure to the sun leads to skin aging. Exposure to UV radiation is the primary factor in external skin aging. It is associated with about 80% of facial skin aging. In contrast to the thin epidermis of externally aged skin, the internally aged epidermis is thick. The outermost layer of the epidermis is most vulnerable due to corneocyte desmosome degradation damage. The expression of the involucrin variability marker in this layer is increased, which is related to the differentiation process of epidermal keratinocytes, and it is damaged by UV light. In basal cells, the expression of the surface protein Beta1-integrin, which binds to ECM (extracellular matrix) proteins, is greatly reduced,
Type VII collagen expression in keratinocytes is reduced in areas of the skin exposed to UV radiation. Type VII collagen forms fibrils that bind the epidermis and dermis together. Reduction in its production affects the formation of wrinkles. Studies have shown that type I collagen breaks down in externally aged skin due to accelerated degradation. Many MPP proteinases, serine proteases and other proteases contribute to this degradation. A distinct feature of photo-aged skin is the accumulation of abnormal elastic tissue deep in the dermis, a pathological phenotype called solar elastosis. UV irradiation increases the expression of elastin 4-fold, which causes elastolysis and characteristic cleavage by the above-mentioned proteases. MMP-2, MMP-3, MMP-7, MMP-9, MMP-12, neutrophil serine protease and human leukocyte elastase are able to degrade elastin. A recent study showed that photoaging causes the N-terminal and central elements of tropoelastin molecules to be more susceptible to cleavage, thus degrading faster.

 

Autorzy:
Shoubing Zhang

Department of Histology and Embryology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China
Central laboratory of Molecular and Cellular Biology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China

Enkui Duan

State Key Lab of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China