Mar 30

_LEARN

/

REFERENCE LAB

Cell Turnover & Why It Slows As We Age

Every time you bounce back from a sunburn or notice an old scar beginning to fade, you have skin cell turnover to thank. As a self-healing organ, skin has incredible regenerative properties thanks to stem cells that are continuously renewing throughout our lifetime. But as you get older, you might notice it takes longer to heal from a scratch–signaling that your skin cell turnover is slowing. But why? Let’s take a closer look at skin cell turnover, why it decreases with age, and what we can do to supercharge our skin’s natural repair potential.







_LEARN

/

REFERENCE LAB

Mar 30

Cell Turnover & Why It Slows As We Age

Every time you bounce back from a sunburn or notice an old scar beginning to fade, you have skin cell turnover to thank. As a self-healing organ, skin has incredible regenerative properties thanks to stem cells that are continuously renewing throughout our lifetime. But as you get older, you might notice it takes longer to heal from a scratch–signaling that your skin cell turnover is slowing. But why? Let’s take a closer look at skin cell turnover, why it decreases with age, and what we can do to supercharge our skin’s natural repair potential.







01 How Does Skin Cell Turnover Work?

Found in the basal layer of the epidermis, skin stem cells actively help repair the skin throughout our lifetimes. These basal cells are continuously dividing, creating new cells in the process. As more and more new cells are produced, they push older ones to the surface of the skin where they are eventually shed as dead skin cells.¹

The rate at which this happens depends largely on age. In young adults, a cell’s transit from the basal layer to the surface may only take 20 days. In older adults, it may take upwards of 30 days. This increased time is a result of diminished cell proliferation at the basal layer. Interestingly, this decline in cell renewal does not occur at a constant rate throughout our lifetimes, but rather remains relatively constant and then drops dramatically after age 50.²

02 What Causes Reduced Cell Turnover?

The key to understanding why this happens requires a close look at one of the central hallmarks of skin aging – cellular senescence. By measuring a key marker of cellular senescence (H2A.J), scientists have observed an age-related increase in senescent cells in all layers of the epidermis, including the basal layer where stem cells are located. When the number of senescent cells increases in this layer, stem cells are no longer able to regenerate as efficiently, leading to a functional decline in stem cell turnover.³


https://www.nature.com/articles/s41514-021-00060-z

03 What Does Slower Cell Turnover Look Like?

With fewer fresh skin cells being created in the basal layer, the skin repairs itself less efficiently and the entire epidermis begins to thin.³ This means that the skin holds onto damaged cells for longer, which can result in telltale signs of aging like dark spots and dullness. Plus, a decrease in epidermal thickness means the skin has less elasticity and bounce, resulting in wrinkles and skin laxity.

04 How the OS-01 Peptide Combats the Decline in Cell Turnover

By maintaining healthy cell turnover as we age, we can ward off signs of epidermal thinning and keep our skin healthy. While many topical products claim to do this by exfoliating the top layer of skin, few actually address the root cause of slowing cell turnover: cellular senescence.

Our OS-01 peptide is different. By targeting cellular senescence, the OS-01 peptide has been scientifically proven to promote an increase in a key cell proliferation marker, MKI67, in the dermis and epidermis of ex vivo human skin samples (Zonari, et al). This shows that the OS-01 peptide can help support healthy cell turnover and maintain our skin’s innate ability to repair itself throughout our lifetimes.

05Key Takeaways

  • Skin repairs damage by proliferating stem cells in the basal layer of the epidermis. This is called skin cell turnover.
  • As we age, the rate that our skin can repair itself decreases from 20 days to over 30 days.
  • This slowing likely occurs because of an increase in cellular senescence in the epidermal layers, making it difficult for stem cells to work as efficiently. With fewer fresher skin cells, the entire epidermis begins to thin–causing wrinkles and other signs of aging.
  • By targeting cellular senescence, the OS-01 peptide has been scientifically proven to promote an increase in a key cell proliferation marker in ex vivo human skin samples (Zonari, et al).
References

01 How Does Skin Cell Turnover Work?

Found in the basal layer of the epidermis, skin stem cells actively help repair the skin throughout our lifetimes. These basal cells are continuously dividing, creating new cells in the process. As more and more new cells are produced, they push older ones to the surface of the skin where they are eventually shed as dead skin cells.¹

The rate at which this happens depends largely on age. In young adults, a cell’s transit from the basal layer to the surface may only take 20 days. In older adults, it may take upwards of 30 days. This increased time is a result of diminished cell proliferation at the basal layer. Interestingly, this decline in cell renewal does not occur at a constant rate throughout our lifetimes, but rather remains relatively constant and then drops dramatically after age 50.²

02 What Causes Reduced Cell Turnover?

The key to understanding why this happens requires a close look at one of the central hallmarks of skin aging – cellular senescence. By measuring a key marker of cellular senescence (H2A.J), scientists have observed an age-related increase in senescent cells in all layers of the epidermis, including the basal layer where stem cells are located. When the number of senescent cells increases in this layer, stem cells are no longer able to regenerate as efficiently, leading to a functional decline in stem cell turnover.³


https://www.nature.com/articles/s41514-021-00060-z

03 What Does Slower Cell Turnover Look Like?

With fewer fresh skin cells being created in the basal layer, the skin repairs itself less efficiently and the entire epidermis begins to thin.³ This means that the skin holds onto damaged cells for longer, which can result in telltale signs of aging like dark spots and dullness. Plus, a decrease in epidermal thickness means the skin has less elasticity and bounce, resulting in wrinkles and skin laxity.

04 How the OS-01 Peptide Combats the Decline in Cell Turnover

By maintaining healthy cell turnover as we age, we can ward off signs of epidermal thinning and keep our skin healthy. While many topical products claim to do this by exfoliating the top layer of skin, few actually address the root cause of slowing cell turnover: cellular senescence.

Our OS-01 peptide is different. By targeting cellular senescence, the OS-01 peptide has been scientifically proven to promote an increase in a key cell proliferation marker, MKI67, in the dermis and epidermis of ex vivo human skin samples (Zonari, et al). This shows that the OS-01 peptide can help support healthy cell turnover and maintain our skin’s innate ability to repair itself throughout our lifetimes.

05Key Takeaways

  • Skin repairs damage by proliferating stem cells in the basal layer of the epidermis. This is called skin cell turnover.
  • As we age, the rate that our skin can repair itself decreases from 20 days to over 30 days.
  • This slowing likely occurs because of an increase in cellular senescence in the epidermal layers, making it difficult for stem cells to work as efficiently. With fewer fresher skin cells, the entire epidermis begins to thin–causing wrinkles and other signs of aging.
  • By targeting cellular senescence, the OS-01 peptide has been scientifically proven to promote an increase in a key cell proliferation marker in ex vivo human skin samples (Zonari, et al).
References

Reviewed by Alessandra Zonari, PhD, Chief Scientific Officer (CSO) and Co-Founder of OneSkin

Alessandra earned her Master’s degree in stem cell biology, and her PhD in skin regeneration and tissue engineering at the Federal University of Minas Gerais in Brazil in collaboration with the 3B’s Research Group in Portugal. Alessandra did a second post-doctoral at the University of Coimbra in Portugal. She is a co-inventor of three patents and has published 20 peer-reviewed papers in scientific journals.

Reviewed by Alessandra Zonari, PhD, Chief Scientific Officer (CSO) and Co-Founder of OneSkin

Alessandra earned her Master’s degree in stem cell biology, and her PhD in skin regeneration and tissue engineering at the Federal University of Minas Gerais in Brazil in collaboration with the 3B’s Research Group in Portugal. Alessandra did a second post-doctoral at the University of Coimbra in Portugal. She is a co-inventor of three patents and has published 20 peer-reviewed papers in scientific journals.

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