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Recent years have seen a fervent pursuit of the elusive fountain of youth. Undoubtedly, individuals are embarking on a journey to rewind time and effectively address the tangible manifestations of skin aging: diminished elasticity, wrinkles, and those persistent dark spots.
Here is the latest trend in Vietnam’s anti-aging treatment market: The booming of Botox to laser treatments and microneedling to chemical peels. People driven by the desire to quickly attain aesthetic enhancements pour money into these therapies. So the question here is why do people start spending tremendous amounts of money on these therapies and whyare they so afraid of aging? Today let’s momentarily set these thoughts aside. Today, our focus shifts towards gaining a holistic comprehension of the underlying skin aging causes and the intricate scientific mechanisms that orchestrate this natural phenomenon.
SKIN AGING Odyssey starts from here!
(for where it starts and where we start our topic)
From the moment of our birth, the aging process begins its subtle journey within our organs, sparing none, not even the skin. The skin, our body’s steadfast guardian against elements, does not elude the passage of time. Instead, it stands as a canvas where the signs of aging gently unveil themselves - a canvas adorned with the delicate marks of reduced elasticity, the stories etched by wrinkles, and the narratives told through the emergence of dark spots.
Aging is progressive reduction in normal tissue function and a deficient response to injury.
Before jumping into the causes of skin aging, let’s take a quick look back on skin structure. Skin can be divided into three layers, going inwards from the outermost layers being the, epidermis, dermis, and subcutaneous tissues.
Epidermis layer consists of keratinocytes, pigment-producing melanocytes, antigen-presenting Langerhans cells, and Merkel cells. This layer is responsible for the skin's texture and hydration, and as we age, its barrier function can become compromised. The gradual reduction in cell turnover and the diminishing capacity to retain moisture contribute to the appearance of fine lines, dullness, and rough texture.
Epidermal-dermal junction (DEJ) is the basement between the epidermis and dermis, primarily containing extracellular proteins produced by fibroblasts below.
Dermis layer is a dynamic layer brimming with collagen, elastin fibers, and a network of blood vessels. This layer comprises primarily fibroblasts, providing an interconnected extracellular matrix of collagenous and elastic fibers.
Collagen, the protein responsible for skin firmness, decreases with age, leading to the loss of elasticity and the formation of wrinkles. Elastin fibers, essential for skin elasticity, also decline over time, contributing to sagging and laxity. The dermis also houses fibroblasts, cells crucial for collagen production, and their activity diminishes as years go by.
Collagen type I is the most abundant protein in skin and alone accounts for 60 to 80% of collagens, along with other extracellular matrix proteins such as collagens (III, V, and VII), elastin proteoglycans, fibronectin, etc.
Subcutaneous tissue is primarily composed of fat cells that provide insulation, cushioning, and support, maintaining the skin’s suppleness and plumpness. As we age, these fat cells decrease in size and number, leading to a loss of volume and contour, especially in areas like the cheeks and temples.
What happens in SKIN-AGING?
The causes of skin aging can be categorized into two primary factors: intrinsic and extrinsic. Intrinsic aging is an inevitable genetic determination process that leads to thin and dry skin, fine wrinkles, and a gradual reduction in dermal volume. On the other hand, extrinsic aging is influenced by external environmental factors such as UV exposure, pollution, smoking, and inadequate nutrition. This type of aging contributes to the development of coarse wrinkles, diminished elasticity, sagging, and a rough-textured appearance. Studies have shown the substantial influence of extrinsic factors on skin aging, with UV exposure alone accounting for around 80% of these effects while intrinsic factors contribute to a mere 3% of the overall aging process.
Intrinsic aging
Intrinsic skin aging also referred to as chronological aging, is primarily attributed to genetic and metabolic processes occurring within sun-protected regions. The alterations seen in intrinsic aging encompass cellular senescence as well as the decline of crucial extracellular matrix constituents such as elastin, collagen, and fibrillin, along with oligosaccharides.
Cell senescence: is characterized by the diminished ability of cells to undergo proliferation. In the context of aging, this decline in proliferation within the basal layer has pronounced histological consequences. The notable effect of reduced basal cell proliferation is the thinning of the epidermis, which, in turn, diminishes the contact surface area between the epidermis and the dermis. Consequently, this reduction in contact area results in a limited space for nutritional exchange, further exacerbating the decline in basal cell proliferation.
So now, let's discuss more cell senescence and the underlying triggers of this process. Extensive studies have pinpointed the role of telomere shortening and damage as major catalysts for both cell senescence and skin aging. But what are telomeres? TELOMERES are akin to protective sentinels, composed of repetitive nucleotide sequences that safeguard the chromosome ends from degradation and abnormal recombination. Telomeres wield multiple protective functions, including preventing chromosomes from unraveling or deteriorating, and shielding them from fusing together, preventing chromosomes from being malfunctioned. In essence, they shield the DNA's crucial gene information. However, here's the twist: after each cell division, telomeres gradually become shorter. Think of it as a countdown: after around 40 to 50 divisions, these telomeres become critically shortened. This brings us to the concept of the Hayflick limit—an intriguing constraint.
While cells divide to facilitate growth and tissue repair, they can only do so a finite number of times, typically around 50 divisions.
Many studies have found evidence for the link between telomere shortening and cell diviaion in senescence. Human keratinocytes undergo replicative senescence after approximately 50 to 1000 population doublings. During this process, they become permanently arrested in the G1 phase of the cell cycle. It is at this juncture that telomere shortening occurs, triggering DNA damage without protective measures. This marks the inception of aging signs.
Extracellular Matrix (ECM) and oligosaccharide decline: As we aged, fibroblasts decline both in terms of quality and quantity, resulting in alterations and degradation of ECM and thus, the skin structure evolves, manifesting in dermal thinning, heightened wrinkling, and a discernible loss of elasticity. It is explained that collagen type I and III exhibit reductions, subsequently influencing the delicate balance between collagen types I and III. This equilibrium is guided by the intricate dance of TGF-β/Smad signaling, which experiences downregulation. This orchestration extends to its downstream participant, the connective tissue growth factor, recognized as a pivotal regulator of collagen expression.
A lipid processing decline, as well as a decrease in the epidermal levels of CD44 glycoprotein, a regulator of keratinocytes proliferation, and the maintenance of local hyaluronic acid homeostasis, have been shown to contribute to this decline.
Overall, the pace of cell proliferation diminishes, resulting in a slowdown of metabolic and biophysical processes within the skin. These changes not only impact the skin's functionality but also have implications for its aesthetic appearance.
Extrinsic aging
Extrinsic aging is often referred to as photoaging due to its association with UV exposure, which accounts for a substantial portion of skin aging, as highlighted below—around 80%. In contrast to the thinning of the epidermis seen in intrinsic aging, extrinsically-aged skin experiences epidermal thickening. This can be attributed to the significant impact of UV exposure on the outermost layer, the stratum corneum. Consequently, the process of desquamation or turnover slows down, resulting in a less effective removal of dead skin cells, due to the compromised degradation of corneocyte desmosomes. The skin's rough texture is influenced not only by alterations in the stratum corneum, but also by changes in the glycosaminoglycan (GAG) content of the skin. While there exist conflicting outcomes regarding whether GAG content increases or decreases, the pivotal aspect to recognize is that GAG doesn't deposit within the papillary dermis, instead, it accumulates on aberrant elastotic material, rendering it ineffective as a source of hydration. This accumulation contributes to the skin's lackluster and leathery appearance.
Note: it also has been found that while hyaluronic acid (HA) is synthesized in both the epidermis and dermis, intrinsically-aged skin witnesses an unchanged content of HA in the dermis while encountering significant diminishes of HA within the epidermis.
Moreover, prolonged exposure to UV radiation leads to a substantial increase in reactive oxygen species (ROS) and a decline in endogenous antioxidant enzymes. Figure below. illustrates the impact of UV radiation, depicting he generation of ROS (primarily from UVA) and DNA damage, primarily from UVA and UVB), respectively, ultimately culminating in skin aging. A more in-depth exploration of the molecular intricacies will be addressed in the subsequent discussion.
Absolutely, the insights we've explored regarding skin aging, its causes, and the internal changes underlying the aging process have set a solid foundation for our future posts. These discussions pave the way for us to delve into topics like active ingredients for combating or slowing down the aging process. By understanding the fundamental mechanisms at play, we can now venture into more specific strategies and solutions to promote healthy and graceful aging.
Stay tuned for more in-depth explorations on this fascinating journey!
Cosmetics x Science
Chloe Vo
References
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