Is your reflection in the mirror showing you the first signs of wrinkles and dark spots? Your days of smooth, radiant, and elastic skin are numbered, and the ticking clock of time and sunlight are to blame.
Skin aging is caused by a combination of natural aging and exposure to sunlight. A little bit of sunshine goes a long way, helping to boost vitamin D levels and keeping seasonal affective disorder at bay. However, soaking up too much is incredibly bad for our skin.
Add to this the inescapable factor of time, and the result is sagging skin, wrinkles, and discolorations: the characteristic signs of skin aging.
Our skin has two distinct layers. The epidermis makes up the outer barrier of our skin and protects us from environmental insults, such as bacteria and ultraviolet (UV) radiation. Meanwhile, the dermis is rich in collagens and other proteins, which are responsible for skin’s strength and elasticity.
Both layers take quite a beating during our lives, and over time, irreparable damage accumulates. But why is skin unable to repair this damage?
The dermis contains a very complex arrangement of extracellular matrix (ECM) proteins, including collagens and others, such as elastin, which provides elasticity.
Fibroblast cells in the dermis not only produce these proteins, but they are also firmly lodged in between these proteins and connected to them. As we age, the ECM progressively loses its integrity as the protein structures become fragmented.
Fibroblasts lose their ECM connections as enzymes slowly degrade the protein networks. This leads to a change in fibroblast shape, severely affecting the cells’ function. Protein production by fibroblasts is reduced, contributing further to the breakdown of the ECM network.
This detrimental circle of events causes a significant reduction in elasticity and results in the loss of our pert skin tone. Why this happens during the normal aging process is not clear, but scientists think that it is caused by a combination of oxidative stress damage to DNA, cell senescence, and chronic inflammation.
However, the dermis is not the only culprit at play.
Although we all experience some natural loss of elasticity and ECM integrity as we age, sun exposure makes this much worse.
But fibroblasts themselves do not react to direct irradiation with UV light in laboratory studies. Instead, scientists think that cells in the epidermis respond to UV exposure by releasing chemicals that diffuse into the dermis and lead to enzyme release in dermal fibroblasts.
This complex interplay is thought to result in deep wrinkles, which is a hallmark of UV-induced skin aging. And recent evidence implicates a third player in causing the signs of skin aging.
As our bodies age, the fat layer below the skin naturally shrinks, resulting in sagging. But until recently, scientists were unable to see any connection between UV damage and fat; UV rays do not penetrate deeply enough to reach the subcutaneous fat.
However, a new type of fat depot in the deep dermis was recently discovered that can penetrate the upper dermis, which is well within reach of UV light.
These specialized fat cells can also respond to chemicals released by cells in the epidermis. In response to chronic UV damage, these fat cells die and are replaced by scar tissue.
Armed with this knowledge, can we avoid the inevitable accumulation of skin damage? Sun exposure at safe levels will certainly limit the amount of damage that UV can inflict on your skin.
As of yet, no one has found an answer to stopping the natural aging process. But rest assured: scientists are continuing their search for the holy grail of aging.
Article Source: https://www.medicalnewstoday.com/articles/318635