Cellular Aging

Cellular aging, or, cellular senescence, is the irreversible process whereby cell divisions are halted but the cell does not die. Senescent cells can be considered to be the opposite of stem cells, rather than having unlimited potential for proliferation these cells are never able to divide again as the process of entering senescence is non-reversible.

Cell Colony

Cell Colony. Image Credit: nobeastsofierce/Shutterstock.com

Cell senescence plays a vital role in protecting the body from cancer, however, the accumulation of these cells has also been linked to several other diseases. Here we discuss these two contrasting roles, as well as the biological underpinnings of cellular aging.

Cellular aging and cancer

Cellular senescence is induced when cells are exposed to sources of oncogenic stress as a response to prevent the development of cancer by ceasing cell proliferation, the hallmark of cancer. Cells cannot be brought out of the senescent phase, once cellular aging is triggered, there are no known stimuli that can trigger it to reenter the cell cycle.

Scientists recognize senescence as one of the body’s major protective strategies against cancer. Cancer can be seen as the unchecked proliferation of cells, often dividing at accelerated rates, and accumulated into tumors. Senescence stops this uncontrolled proliferation, preventing cancer from developing and spreading throughout the body.

Therapeutic approaches to treating cancer can induce senescence, the body’s protective strategy. Drugs used in chemotherapy, as well as ionizing radiation, can induce cellular senescence.

Cancer, as well as neurodegenerative diseases such as Alzheimers disease and Parkinsons disease, can be considered diseases of failed or malfunctioning cell senescence.

Cellular aging and disease

While senescence can induce an anti-tumor effect by slowing growth, it can also be harmful to the body. A mounting body of evidence exists that demonstrates the role of senescence in numerous diseases such as atherosclerosis, cardiac dysfunction, diabetes, Hutchinson–Gilford progeria and Werner syndrome, and general tissue dysfunction.

In this way, senescence can be seen as a double-edged sword, protecting the body on one hand, but on the other, causing disease and aging. Because senescent cells do not die, they merely stop dividing and linger in the body, over time senescent cells can build up. The problem with mounting numbers of senescent cells in the body is that they can release substances that are harmful to the body, and, therefore, in large numbers that can contribute to the development of disease.

The biology of cellular processing

The exact biological processes involved in cellular aging have long been studied, not just because of their links with disease, but also because of their association with the idea of eternal youth. Recently, significant advances have been made in our understanding of senescence in human cells. In particular, the results of a 2019 study conducted by a team of scientists at the USC Viterbi School of Engineering greatly furthered our knowledge of cellular aging, demonstrating for the first time that senescent cells lose the ability to produce nucleotides.

In their groundbreaking study, the team forced young, healthy cells to stop producing nucleotides, known as the building blocks of DNA, and found that in doing so, they forced these young cells into senescence. Their findings revealed that nucleotides are vital for maintaining a cell’s “youth”. The study’s authors theorized that cells could be prevented from entering senescence by preventing the loss of nucleotide synthesis, the impact of which could be that cells age more slowly.

To find out more about this process, the team of researchers observed young cells in the lab and monitored how they processed different molecules. They first watched the cells proliferate, then, fed them molecules that they had labeled with stable carbon isotopes, which allowed them to track how these molecules were processed by distinct biochemical pathways.

The results were developed into 3D images and revealed that two nuclei are a previously unknown hallmark of senescent cells. In addition, they were able to show that senescent cells do not synthesize DNA, a finding which marries up with the previous revelation that senescent cells stop producing nucleotides.

Before this research being published, scientists had focussed on studying senescence in fibroblasts, common cells that form connective tissue in animals. In the study conducted at the USC Viterbi School of Engineering, however, the researchers used epithelial cells, a type of cell found in the skin, blood vessels, urinary tract, and organs. In addition, they are the most common cell type for cancer to initiate. Therefore, their data is particularly relevant to cellular aging concerning cancer, and to inspiring future therapeutic research.

Learning more about cellular aging could be the key to new treatments for cancer and other diseases

Due to its strong links with cancer and other types of disease, growing our knowledge of how senescence occurs in human cells will undoubtedly help develop more effective therapeutic options in the future. The current data is promising and opens up a new avenue of research for scientists working on a wide range of diseases.

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Further Reading

Last Updated: Feb 26, 2021

Sarah Moore

Written by

Sarah Moore

After studying Psychology and then Neuroscience, Sarah quickly found her enjoyment for researching and writing research papers; turning to a passion to connect ideas with people through writing.

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