‘Zombie’ cells are still alive but unable to function and they accumulate with age

(ORDO NEWS) — Damage to the ends of chromosomes can lead to the formation of “zombie cells” that are still alive but unable to function, according to a recently published study in the journal Nature Structural and Molecular Biology.

As cells prepare to divide, their DNA coils tightly around proteins to form chromosomes, which provide structure and support for the genetic material. At the ends of chromosomes are repetitive stretches of DNA called telomeres, which form a protective cap that prevents damage to the genetic material.

However, telomeres shorten with each cell division. This means that with age, as cells divide more and more often, telomeres become shorter and more likely to lose their ability to protect DNA.

Damage to the genetic material can lead to mutations that cause cells to divide uncontrollably, leading to cancer.

However, cells avoid cancer when their telomeres become too short after they divide too many times and potentially accumulate damage along the way, entering a zombie-like state that stops cells from dividing through a process called cellular aging.

Because they are resistant to death, senescent – or “zombified” – cells accumulate with age. They may be beneficial to health by promoting aging of nearby cells at risk of becoming cancerous and by recruiting immune cells to destroy cancer cells.

But they can also promote disease by disrupting tissue healing and immune function, and by releasing chemicals that promote inflammation and tumor growth.

We wanted to see if direct damage to telomeres could be enough to kick-start the aging process and create zombie cells. To find out, we needed to limit the damage to telomeres only.

So we attached the protein to the telomeres of human cells grown in the lab. We then added a dye to the protein, which made it sensitive to light.

Far-red light (or light with a wavelength slightly shorter than infrared) induces the protein to produce free oxygen radicals – highly reactive molecules that can damage DNA – right at the telomeres, sparing the rest of the chromosome and the cell.

We found that direct damage to the telomeres was enough to turn the cells into zombies, even if these protective caps were not shortened. The reason for this, as we found out, most likely lies in the disruption of DNA replication in telomeres, which makes chromosomes even more susceptible to damage and mutation.

Why is it important

Telomeres naturally shorten with age. They limit the number of cell divisions, signaling the cells to become zombies when they reach a certain length.

But excess free radicals, both from normal bodily processes and from exposure to harmful chemicals like air pollution and tobacco smoke, can lead to a condition called oxidative stress, which can speed up telomere shortening.

This can prematurely start the aging process and contribute to the development of age-related diseases, including immunodeficiency, cardiovascular disease, metabolic disease and cancer.

Our research shows that telomeres serve not only as an alarm clock that a cell has been dividing too many times, but also as a warning call for harmful levels of oxidative stress. Age shortening of telomeres is not the only thing that triggers the aging process; telomere damage is also enough to turn a cell into a zombie.

What other research is being done

Researchers are exploring therapies and interventions that can protect telomeres from damage and prevent the accumulation of zombie cells. A number of studies in mice have found that removing zombie cells can promote healthy aging by improving cognition, muscle mass and function, and recovery from viral infections.

Researchers are also developing drugs called senolytics that can either kill zombie cells or prevent them from reappearing.

What’s next

This study focuses on the consequences of telomere damage in actively dividing cells such as kidney and skin cells. We are now studying how this damage will affect cells that do not divide, such as neurons or heart muscle cells.

Although researchers have shown that telomeres in non-dividing cells and tissues become increasingly dysfunctional with age, it is not clear why this happens, as telomeres should not shorten in the first place.


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