Science
Gesponsert
What are zombie cells and how are they related to aging?
To get his own take on this, we asked a molecular biologist to weigh in.
National Cancer Institute
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Research has been trying to determine exactly what is behind the aging process for some time and has largely linked this fact to a biological factor: senescent cells, also known as zombie cells.
During cell division, a single cell divides into two daughter cells, with the genetic material being evenly distributed among the daughter cells. Because this process is so important, these steps are carefully controlled by specific genes. If this fundamental process is not properly managed, health problems such as cancer can result.
Zombie cells or senescent cells are cells that no longer divide. In a younger body, the immune system recognizes these cells and eliminates them. With increasing age, however, the immune system is no longer able to cope with this task as well.
A recently published study links zombie cells to age-related diseases such as cancer, dementia and heart disease and reveals how these cells are formed. The study found that oxidative damage (damage caused by an imbalance between free radicals and antioxidants in the body) to telomeres, the protective ends of chromosomes, could trigger the formation of zombie cells.
Scientists have been analyzing these cells and their significance for the aging process for years. We asked molecular biologist Dr. Daniel Wallerstorfer, who has his own assumption about zombie cells.
What are zombie cells and what do they do?
Zombie cells, or rather “sleeping” cells as I like to call them, are cells that have grown old at the end of their life cycle. Instead of dying, they go into a state of sleep and remain in the tissue. This is a problem for a number of reasons:
They no longer perform their actual function and are therefore just useless ballast for the body.
Since they are already very old, there is a high risk that their DNA could change and become cancer cells.
There is also evidence that they may even damage those around them.
Does everyone have zombie cells?
Yes And the older we get, the more common they become in the body. One of the reasons why we age as humans.
How are zombie cells related to aging?
Human genes are hidden in DNA. We have 23,000 different genes that sit on long DNA strands and perform their functions there. These DNA strands must be organized in the cell. To do this, the cell wraps them up into very compact structures, the so-called Chromosomes (those X-shapes that you know from biology lessons). With every cell division, however, the entire DNA must be copied and thus doubled so that each daughter cell receives the entire set of genes.
Now comes the problem. During every copying process, small parts of the chromosome ends break away. To prevent this from immediately causing chaos in the cell, we have excess, meaningless DNA at the ends of the chromosomes that doesn't matter whether it breaks away. This DNA is called the so-called telomeres.
Cells have about enough such telomere reserve DNA so that they can divide 50 to 70 times. This also means that the older we get, the more often our cells have divided and the shorter the telomeres become. After 50-70 divisions (the so-called “Hayflick Limit”), these are therefore used up and the vital genes suddenly start to break away. The cell has reached the end of its life span and then becomes a zombie cell.
What can you do to prevent/slow down the formation of zombie cells?
Anything that preserves the length of telomeres reduces or delays the formation of these cells. There are certain types of diet, such as the Mediterranean diet, that are helpful. However, these diets only work for people who also have other specific genetic defects (we analyse something like that in our laboratory).
Could researching zombie cells be the key to a longer life?
My GUESS was then and still is today that if you could manage to kill the zombie cells (either with a targeted drug or by genetically modifying the human that installs a suicide mode in zombie cells), this aging aspect could be reduced or “cured”. But this is a drastic intervention in the body and ethically tricky.
Alternatively, we could focus on therapies to lengthen telomeres so that the cells do not even reach the age limit in the first place. But that in turn is a risk. Because it is assumed that this “Hayflich Limit” is an important protection against cancer. This is because a tumour cell starts dividing immediately and loses telomeres, just like normal cells. Once these have been used up, the entire tumor goes into sleep/zombie mode and cancer was prevented as a result. Switching this off completely would therefore probably drastically increase the cancer rate.
References
- How do cells divide? : MedlinePlus Genetics. (n.d.). https://medlineplus.gov/genetics/understanding/howgeneswork/cellsdivide/
- Barnes, R.P., De Rosa, M., Thosar, S.A., Detwiler, A.C., Roginskaya, V., Van Houten, B., Bruchez, M.P., Stewart-Ornstein, J. & Opresko, P.L. (2022). Telomeric 8-oxo-guanine drives rapid premature senescence in the absence of telomere shortening. Nature Structural & Molecular Biology, 29(7), 639—652. https://doi.org/10.1038/s41594-022-00790-y
- Van Deursen, J.M. (2014). The role of senescent cells in aging. Nature, 509(7501), 439—446. https://doi.org/10.1038/nature13193
Publiziert
17.3.2024
Kategorie
Science
Scientific Terms
Chromosome
The compact structure in which a cell's DNA is organized and which is held together by proteins. The genomes of the various organisms are arranged in a different number of chromosomes. Human cells have 23 pairs.
DNA
Abbreviation for deoxyribonucleic acid, the molecule that encodes the information that a cell needs to function or a virus needs to replicate. Forms a double helix that resembles a twisted ladder, similar to a zipper. The bases, abbreviated as A, C, T, and G, are on either side of the ladder or strand that run in opposite directions. The bases exert an attraction on each other so that A sticks to T and C to G. The sequence of these letters is known as the genetic code.
Gene
A section of DNA that encodes the information needed to make a protein. Each gene is a set of instructions for making a specific molecular machine that helps a cell, an organism, or a virus to function.
Seneszens
Latin senescere “getting old”, “aging”
The process of deterioration with age.
Telomere/Telomere Loss
Gr. Télos' Ende 'and' Télos' Teil '
A telomere is a cap that protects the end of the chromosome from wear and tear, comparable to the awl on the end of a shoelace or the burnt end of a rope to prevent fraying. As we age, telomeres erode to the point where the cell reaches the Hayflick limit. This is the point at which the cell sees the erosion as a break in DNA, stops dividing and becomes senescent.
Cellular Senescence
The process that occurs when normal cells stop dividing and start releasing inflammatory molecules, sometimes caused by telomere shortening, DNA damage, or epigenomic noise. Despite their apparent “zombie” state, senescent cells remain alive and damage neighboring cells with their inflammatory secretions.
Research has been trying to determine exactly what is behind the aging process for some time and has largely linked this fact to a biological factor: senescent cells, also known as zombie cells.
During cell division, a single cell divides into two daughter cells, with the genetic material being evenly distributed among the daughter cells. Because this process is so important, these steps are carefully controlled by specific genes. If this fundamental process is not properly managed, health problems such as cancer can result.
Zombie cells or senescent cells are cells that no longer divide. In a younger body, the immune system recognizes these cells and eliminates them. With increasing age, however, the immune system is no longer able to cope with this task as well.
A recently published study links zombie cells to age-related diseases such as cancer, dementia and heart disease and reveals how these cells are formed. The study found that oxidative damage (damage caused by an imbalance between free radicals and antioxidants in the body) to telomeres, the protective ends of chromosomes, could trigger the formation of zombie cells.
Scientists have been analyzing these cells and their significance for the aging process for years. We asked molecular biologist Dr. Daniel Wallerstorfer, who has his own assumption about zombie cells.
What are zombie cells and what do they do?
Zombie cells, or rather “sleeping” cells as I like to call them, are cells that have grown old at the end of their life cycle. Instead of dying, they go into a state of sleep and remain in the tissue. This is a problem for a number of reasons:
They no longer perform their actual function and are therefore just useless ballast for the body.
Since they are already very old, there is a high risk that their DNA could change and become cancer cells.
There is also evidence that they may even damage those around them.
Does everyone have zombie cells?
Yes And the older we get, the more common they become in the body. One of the reasons why we age as humans.
How are zombie cells related to aging?
Human genes are hidden in DNA. We have 23,000 different genes that sit on long DNA strands and perform their functions there. These DNA strands must be organized in the cell. To do this, the cell wraps them up into very compact structures, the so-called Chromosomes (those X-shapes that you know from biology lessons). With every cell division, however, the entire DNA must be copied and thus doubled so that each daughter cell receives the entire set of genes.
Now comes the problem. During every copying process, small parts of the chromosome ends break away. To prevent this from immediately causing chaos in the cell, we have excess, meaningless DNA at the ends of the chromosomes that doesn't matter whether it breaks away. This DNA is called the so-called telomeres.
Cells have about enough such telomere reserve DNA so that they can divide 50 to 70 times. This also means that the older we get, the more often our cells have divided and the shorter the telomeres become. After 50-70 divisions (the so-called “Hayflick Limit”), these are therefore used up and the vital genes suddenly start to break away. The cell has reached the end of its life span and then becomes a zombie cell.
What can you do to prevent/slow down the formation of zombie cells?
Anything that preserves the length of telomeres reduces or delays the formation of these cells. There are certain types of diet, such as the Mediterranean diet, that are helpful. However, these diets only work for people who also have other specific genetic defects (we analyse something like that in our laboratory).
Could researching zombie cells be the key to a longer life?
My GUESS was then and still is today that if you could manage to kill the zombie cells (either with a targeted drug or by genetically modifying the human that installs a suicide mode in zombie cells), this aging aspect could be reduced or “cured”. But this is a drastic intervention in the body and ethically tricky.
Alternatively, we could focus on therapies to lengthen telomeres so that the cells do not even reach the age limit in the first place. But that in turn is a risk. Because it is assumed that this “Hayflich Limit” is an important protection against cancer. This is because a tumour cell starts dividing immediately and loses telomeres, just like normal cells. Once these have been used up, the entire tumor goes into sleep/zombie mode and cancer was prevented as a result. Switching this off completely would therefore probably drastically increase the cancer rate.
Referenzen
- How do cells divide? : MedlinePlus Genetics. (n.d.). https://medlineplus.gov/genetics/understanding/howgeneswork/cellsdivide/
- Barnes, R.P., De Rosa, M., Thosar, S.A., Detwiler, A.C., Roginskaya, V., Van Houten, B., Bruchez, M.P., Stewart-Ornstein, J. & Opresko, P.L. (2022). Telomeric 8-oxo-guanine drives rapid premature senescence in the absence of telomere shortening. Nature Structural & Molecular Biology, 29(7), 639—652. https://doi.org/10.1038/s41594-022-00790-y
- Van Deursen, J.M. (2014). The role of senescent cells in aging. Nature, 509(7501), 439—446. https://doi.org/10.1038/nature13193
Publiziert
17.3.2024
Kategorie
Science
Wissenschaftliche Begriffe
Chromosome
The compact structure in which a cell's DNA is organized and which is held together by proteins. The genomes of the various organisms are arranged in a different number of chromosomes. Human cells have 23 pairs.
DNA
Abbreviation for deoxyribonucleic acid, the molecule that encodes the information that a cell needs to function or a virus needs to replicate. Forms a double helix that resembles a twisted ladder, similar to a zipper. The bases, abbreviated as A, C, T, and G, are on either side of the ladder or strand that run in opposite directions. The bases exert an attraction on each other so that A sticks to T and C to G. The sequence of these letters is known as the genetic code.
Gene
A section of DNA that encodes the information needed to make a protein. Each gene is a set of instructions for making a specific molecular machine that helps a cell, an organism, or a virus to function.
Seneszens
Latin senescere “getting old”, “aging”
The process of deterioration with age.
Telomere/Telomere Loss
Gr. Télos' Ende 'and' Télos' Teil '
A telomere is a cap that protects the end of the chromosome from wear and tear, comparable to the awl on the end of a shoelace or the burnt end of a rope to prevent fraying. As we age, telomeres erode to the point where the cell reaches the Hayflick limit. This is the point at which the cell sees the erosion as a break in DNA, stops dividing and becomes senescent.
Cellular Senescence
The process that occurs when normal cells stop dividing and start releasing inflammatory molecules, sometimes caused by telomere shortening, DNA damage, or epigenomic noise. Despite their apparent “zombie” state, senescent cells remain alive and damage neighboring cells with their inflammatory secretions.
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