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Peptides, Telomeres, and Cellular Senescence – Oh My! Featured

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The phenomenon of aging and the concept of expanding the human lifespan has thrived over the last several decades. The quest for a more youthful appearance has infiltrated research for several generations. The primary causes for accelerated cellular damage or aging were mostly found to be a result of reactive oxidative stress, over-exposure to ultraviolet rays, environmental factors (pollution and toxins), and illnesses. However, further research has provided a deeper understanding to the causes of aging, which includes telomere shortening and cellular senescence. This article will discuss the science of cellular senescence, the role of telomeres, and how peptides are able to assist the cells to decelerate the aging process.

 

THE SCIENCE OF CELLUAR SENESCENCE

Cellular senescence is defined as the cells’ limited capacity of proliferation.1 The term cellular senescence encompasses apoptosis and the declining ability of cellular communication with other cells. Why does this happen? Scientists have discovered many answers to this question; however, further research is needed to understand the full capacity of this phenomenon. One viable answer was discovered by a scientist, Leonard Hayflick, in the mid-1960s.

 

In 1965, Dr. Hayflick discovered that normal human fetal cells divide between 40 and 60 times before entering the senescence phase. His finding refuted the contention that cells are immortal.2 Dr. Hayflick discovered that during cell mitosis, the telomeres on the end of the chromosomes strands shorten slightly, which contributed to overall aging. He identified three phases of life of normal cultured cells: phase one, the primary culture, phase two, the cells proliferate, and phase three, after months of doubling, the cell replication rate slows before halting altogether.2 Subsequently, Hayflick’s finding was coined Hayflick Limit Theory of Aging or, more commonly, the Hayflick Effect.

 

Dr. Hayflick was the first to report that only cancer cells were immortal. He found cancer cells do not develop cellular senescence due to an enzyme called telomerase. The function of telomerase is to extend the telomeres. If telomeres are extended and not shortened, the cancer cells have the ability to replicate indefinitely.2

     

TELOMERES AND CELLULAR SENESCENCE

Telomeres are small segments found at the end of chromosome strands that shorten when cells divide. Their primary role is to preserve the DNA during cellular replication.1 When telomeres shorten, the cell stops reproducing or dividing. Many research findings report telomeres in longer length may extend the lifespan of DNA, allowing the strand to be replicated more times than usual.

 

PEPTIDES’ INFLUENCE ON CELLULAR SENESCENCE

Critical information of cells is stored in the DNA. Without telomeres, chromosomes may fuse together, causing genetic instability. In order to launch protein synthesis, genes have to be activated by triggering molecules or peptides.1 Some peptides match specific parts in the cell’s DNA, following the lock-key principle. As a result, the peptide resumes the synthesis of the protein from which it was originally built. As proteins age, they become fragmented into the original peptide. This is part of the biological feedback loop and is vital to cell life.1

 

The mitochondria also play a critical role in energy production, metabolism, and cellular signaling.3 Bioavailable peptides have the ability to signal the mitochondria and assist with cellular proliferation.

 

Peptides function as specific messengers and are able to assist with energy production or signal cytokines during inflammation. Some bioavailable peptides have the ability to respond to cellular stress and have a range of protective effects. Signaling pathways and cell receptors are identified by the peptides. According to an article published in Aging, peptides assist cells in function, block apoptosis, decrease inflammation, and reduce oxidative stress.3 In summary, bioactive peptides have the ability to align with the natural pathways of the cells to support telomere length.

 

References

1 Harle-Bachor, C. and P. Boukamp. “Telomerase activity in the regenerative basal layer of the epidermis in human skin and in immortal and carcinoma-derived skin keratinocytes.” Proc. Natl. Acad. Sci. 93 (1996): 6476-648.

2 Wikipedia. 2019. “Hayflick limit.” Last modified 20 June 2019. www.wikipedia.org/wiki/hayflick_limit.

3 Su-Jeong, Kim, Hermal Mehta, Junxiang Wan, et al. Aging 10, no. 6 (2018): 1239-1256.

 

Susan Wade 2019Susan Wade is a licensed aesthetician joining Viktoria De’Ann in 2015 as the director of education and sales after being in the health and education industry for over 18 years. She has a master’s in higher education administration and enjoys sharing her wealth of knowledge with physicians, clinicians, and students nationwide. Wade has a diverse background beyond aesthetics as a college instructor in kinesiology and business and is an owner of a successful sports conditioning business’ and a nutrition coach. Her passion lies in understanding the complexities of physiology, nutrition, and biology and in educating practitioners on how to incorporate these areas to reach better solutions and successful results with their clients.

 

 

 

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