How many times a human cell divides. Aging - the price to pay for the suppression of cancerous tumors? Cross-linking theory

26.11.2020

The idea that aging can be laid down from the moment of birth was put forward by the German Darwinian scientist August Weismann (Friedrich Leopold August Weismann, 1834-1914). In his famous lecture in 1891, Weismann proposed that death by old age arose in the course of evolution:<Я рассматриваю смерть не как первичную необходимость, а как нечто приобретенное вторично в процессе адаптации:>.

Approaches to the classification of aging theories

Theories explaining the aging of organisms can be classified in various ways.
For example, there is a division into three groups: genetic theories, in which genetically controlled programmed<биологические часы>, such as telomeres regulate growth, maturity and old age, neuroendocrine theories and damage accumulation theories. Generally speaking, this division is rather conditional, because all these mechanisms are important and interconnected.

There are also 2 large groups: stochastic (probabilistic) theories and programmed aging theories.
It is possible to classify theories according to the level of organization of living matter.
According to V.N. Anisimov, head of the Russian Gerontological Society, the most striking theories are the free radical theory put forward in 1956 by D. Harman (Harman, 1956, 1998), L. Hayflick’s theory of cellular (replicative) aging (Hayflick, Moorhead, 1961; Hayflick, 1998), telomere theory by A.M. Olovnikov (Olovnikov, 1971; Olovnikov, 1996), elevation theory of aging by V.M. Dilman (Dilman, 1987; Dilman, 1971, 1994) and T. Kirkwood's expendable soma theory (Kirkwood, 1997, 2002). the free radical theory put forward in 1956 by D. Harman, the theory of cellular (replicative) aging by L. Hayflick and the telomeric theory by A. M. Olovnikov, the elevation theory of aging by V. M. Dilman.

Classification of theories of stochastic aging

(Schulz-Aellen, 1997)

Somatic Mutation Theory - Somatic mutations disrupt genetic information and reduce cell function
Error catastrophe - Errors in transcription and/or translation processes reduce cell efficiency
DNA damage, DNA repair - DNA damage is constantly being repaired by various mechanisms. Repair efficiency is positively correlated with lifespan and decreases with age
Protein damage - Conformational abnormalities of proteins and enzymes (cross-links) damage cell function
Cross-links - Chemical cross-links of important macromolecules (such as collagen) lead to dysfunction of cells and tissues
Wear and tear - The accumulation of damage in daily life reduces the effectiveness of the body

Classification of theories of programmed aging

(Schulz-Aellen, 1997)

Genetic theories - Aging is caused by programmed changes in gene expression, or by the expression of specific proteins
Death genes - There are cell death genes
Selective death - Cell death is due to the presence of specific membrane receptors
Telomere shortening - Telomere shortening with age in vitro and in vivo leads to chromosome instability and cell death
Disorders of differentiation - Errors in the activation-repression mechanisms of genes, leading to the synthesis of excess, non-essential or unnecessary proteins
Accumulation<загрязнений>- Accumulation of waste products of metabolism reduces cell viability
Neuroendocrine theories - Insufficiency of the nervous and endocrine systems in maintaining homeostasis. Loss of homeostasis leads to aging and death
Immunological theory - Certain alleles can increase or decrease lifespan.
Metabolic theories - Longevity is inversely proportional to metabolic rate
Free radical theory - Longevity is inversely proportional to the degree of free radical damage and directly proportional to the effectiveness of antioxidant systems
Aging Clock - Aging and death are the result of a predetermined biological plan
Evolutionary theories - Natural selection eliminates individuals after they have produced offspring

Classification of the most important theories of aging according to the level of integration

(Yin, Chen, 2005)

Organism level of integration
Wear theory - Sacher, 1966
The Catastrophe Theory of Errors - Orgel, 1963
Stress Injury Theory - Stlye, 1970
The autointoxication theory - Metchnikoff, 1904
Evolutionary theory (programmed aging theory) - Williams, 1957
Information retention theory (programmed aging theory)

Organ level
Endocrine Theory - Korenchevsky, 1961
Immunological Theory - Walford, 1969
Inhibition of the brain

Cellular level
Cell Membrane Theory - Zg-Nagy, 1978
Somatic Mutation Theory - Szillard, 1959
Mitochondrial theory - Miquel et al., 1980
Mitochondrial-Lysosomal Theory - Brunk, Terman, 2002
Cell proliferative limit theory (programmed aging theory) - Hayflick, Moorhead, 1961

Molecular level
DNA damage accumulation theory - Vilenchik, 1970
Trace element theory - Eichhorn, 1979
Free Radical Theory - Harman, 1956
The Theory of Peppered Crosslinks - Bjorksten, 1968
Theory of oxidative stress - Sohal, Allen, 1990; Yu, Yang, 1996
Theory of non-enzymatic glycosylation - Cerami, 1985
Theory of carbonyl intoxication - Yin, Brunk, 1995
Pollution catastrophe theory - Terman, 2001
Theory of gene mutations
Theory of telomere shortening (the theory of programmed aging) - Olovnikov, 1971

Other approaches
Aging as entropy - Sacher, 1967; Bortz, 1986
Mathematical theories and various unified theories - Sohal, Alle, 1990;
Zg-Nagy, 1991; Kowald, Kirkwood, 1994

Denham Harman's Free Radical Theory of Aging

Leonard Hayflick's Theory of Cellular Aging

Elevation theory of aging

It was put forward and substantiated in the early 50s of the last century by the Leningrad scientist Vladimir Dilman. According to this theory, the mechanism of aging begins its work with a constant increase in the threshold of sensitivity of the hypothalamus to the level of hormones in the blood. As a result, the concentration of circulating hormones increases. As a result, various forms of pathological conditions arise, including those characteristic of old age: obesity, diabetes, atherosclerosis, cancryophilia, depression, metabolic immunosuppression, hypertension, hyperadaptation, autoimmune diseases and menopause. These diseases lead to aging and ultimately to death.
In other words, in the body, there is a large biological clock that will count the time of life allotted to it from birth to death. At a certain moment, these clocks trigger destructive processes in the body, which are commonly called aging.
According to Dilman, aging and related diseases are a by-product of the implementation of the genetic program of ontogenesis - the development of the body.
It follows from the ontogenetic model that if the state of homeostasis is stabilized at the level reached by the end of the development of the organism, then it is possible to slow down the development of diseases and natural senile changes and increase the species limits of human life.
Download the book by V. Dilman "Large biological clock"

Theory of consumable (disposable) soma

Cross-linking theory

This aging mechanism is a bit like free radicals. Only the role of aggressive substances here is played by sugars, first of all, glucose, which is always present in the body. Sugars can react chemically with various proteins. In this case, naturally, the functions of these proteins can be disturbed. But what is much worse, sugar molecules, when combined with proteins, have the ability to<сшивать>protein molecules to each other. Because of this, the cells begin to work worse. They accumulate cellular debris.
One of the manifestations of such cross-linking of proteins is the loss of tissue elasticity. Outwardly, the most noticeable is the appearance of wrinkles on the skin. But much more harm comes from the loss of elasticity of blood vessels and lungs. In principle, cells have mechanisms to destroy such crosslinks. But this process requires a lot of energy from the body.
Today, there are already drugs that break down the internal crosslinks and turn them into nutrients for the cell.

Error theory

Hypothesis<старения по ошибке>was put forward in 1954 by the American physicist M. Szilard. Investigating the effects of radiation on living organisms, he showed that the action of ionizing radiation significantly reduces the life span of people and animals. Under the influence of radiation, numerous mutations occur in the DNA molecule and some of the symptoms of aging are initiated, such as gray hair or cancerous tumors. From his observations, Szilard concluded that mutations are the direct cause of the aging of living organisms. However, he did not explain the fact of aging of people and animals that were not exposed to radiation.
His follower L. Orgel believed that mutations in the genetic apparatus of a cell can either be spontaneous or occur in response to aggressive factors - ionizing radiation, ultraviolet radiation, exposure to viruses and toxic (mutagenic) substances, etc. Over time, the DNA repair system wears out, resulting in aging of the body.

Theory of apoptosis (cell suicide)

Academician V.P. Skulachev calls his theory the theory of cellular apoptosis. apoptosis (gr.<листопад>) is the process of programmed cell death. As trees get rid of parts in order to preserve the whole, so each individual cell, having passed its life cycle, must die off and a new one must take its place. If a cell becomes infected with a virus, or a mutation occurs in it leading to malignancy, or simply expires, then in order not to endanger the entire organism, it must die. Unlike necrosis - violent death of cells due to injury, burns, poisoning, lack of oxygen as a result of blockage of blood vessels, etc., during apoptosis, the cell neatly disassembles itself into parts, and neighboring cells use its fragments as a building material.
Mitochondria also undergo self-destruction - having studied this process, Skulachev called it mitoptosis. Mitoptosis occurs when too many free radicals are produced in the mitochondria. When the number of dead mitochondria is too high, their decay products poison the cell and lead to its apoptosis. Aging, from the point of view of Skulachev, is the result of the fact that more cells die in the body than are born, and dying functional cells are replaced by connective tissue. The essence of his work is the search for methods to counteract the destruction of cellular structures by free radicals. According to the scientist, old age is a disease that can and should be treated, the body's aging program can be disabled and thereby turn off the mechanism that shortens our life.
According to Skulachev, the main reactive oxygen species that leads to the death of mitochondria and cells is hydrogen peroxide. Currently, under his leadership, the drug SKQ, designed to prevent signs of aging, is being tested.
Interview with Novaya Gazeta

Adaptive-regulatory theory

The aging model developed by the outstanding Ukrainian physiologist and gerontologist V.V. Frolkis in the 1960s and 70s is based on the widely held notion that old age and death are genetically programmed.<Изюминка>Frolkis's theory is that age-related development and life expectancy are determined by the balance of two processes: along with the destructive process of aging, the process<антистарения>, for which Frolkis proposed the term<витаукт>(lat. vita - life, auctum - increase). This process is aimed at maintaining the viability of the body, its adaptation, and increasing life expectancy. Ideas about anti-aging (vitaukte) have become widespread. Thus, in 1995, the first international congress on this problem was held in the United States.
An essential component of Frolkis's theory is the gene-regulatory hypothesis developed by him, according to which the primary mechanisms of aging are disturbances in the work of regulatory genes that control the activity of structural genes and, as a result, the intensity of the synthesis of proteins encoded in them. Age-related violations of gene regulation can lead not only to a change in the ratio of synthesized proteins, but also to the expression of previously inactive genes, the appearance of previously unsynthesized proteins, and, as a result, to aging and cell death.
VV Frolkis believed that the gene-regulatory mechanisms of aging are the basis for the development of common types of age-related pathology - atherosclerosis, cancer, diabetes, Parkinson's and Alzheimer's diseases. Depending on the activation or suppression of the functions of certain genes, this or that aging syndrome, this or that pathology will develop. Based on these ideas, the idea of gene regulatory therapy was put forward, designed to prevent the shifts underlying the development of age-related pathology.

Olovnikov's redusom theory

The protein-coated linear redusome DNA molecule is a copy of a segment of chromosomal DNA. nest. Like telomeric DNA, redusome linear DNA shortens over time. Therefore, tiny redusomes progressively decrease in size; hence their name. Along with the loss of DNA in the redusome, the number of different genes contained in it also decreases. The shortening of redusomal DNA molecules (and the resulting change in the set of genes in redusomes) changes the level of expression of various chromosomal genes with age and, therefore, serves as a key means of measuring biological time in individual development.

In 1882, the German biologist A. Weismann postulated in his work that somatic cells are capable of a limited number of divisions, which is the reason for the limited life span. The different life span of animals was explained by him by the different number of possible cell divisions. His idea of depleting the ability of cells to divide with age became very popular.

In 1912-1913, A. Carrel and A. Ebeling, based on experiments with chicken heart fibroblasts outside the body, showed that, under appropriate conditions, cells can multiply almost unlimitedly. In the scientific world, the opposite idea has been established that the somatic cells that make up the mortal organism are potentially immortal.

Therefore, the reasons for the limitation of life expectancy began to be sought at the supracellular physiological level, including at the level of hormonal regulation. The popularity of this idea was very high, so the various exceptions to this "rule" were simply ignored.

E. Swim in 1956, after studying many works and conducting his own research, decided to revise the teachings of Carrel. He came to the conclusion that cells capable of unlimited division undergo nonspecific degeneration. An important conclusion was also drawn that cell proliferation cessation is not a methodological artifact due to factors such as inoculum size, toxic environment, or inability of cells to proliferate on glass. Cells have a limit on the number of divisions. However, it was not easy to defeat the old concept.

In the 60s and 70s, L. Hayflick published a series of scientific and popular science articles on the results of long-term cultivation of human fibroblasts. His papers confirmed Swim's findings and aroused great interest and wide publicity. This phenomenon is called the Hayflick limit.

What is the reason for the restriction of cell division? Is there a cell division counter? The cells of the tissues of the body are specialized and some, in the process of their differentiation, simply lose the ability to divide, for example, nerve cells. With age, cellular structures wear out, repair mechanisms (recovery), a complex system of cell mitosis work with less intensity.

Certainly, this is the case. Relatively recently, attention was paid to the dependence of the length of chromosome telomeres and human age. Telomeres are the ends of chromosomes. It turned out that the older the person, the shorter their average length. Each cell division leads to a decrease in the length of telomeres, which is explained by the mechanism of chromosome duplication, to be precise, the specifics of the polymerase.

It has been experimentally demonstrated that an increase in telomere length leads to an increase in the number of cell divisions. A large number of different genes are collected around the telomere region. It is quite possible that a change in telomere length is reflected in the expression of certain regions located near the telomere. Currently, the study of these areas is quite active.

Have you ever wondered why cancer cells are physiologically young and have the ability to endlessly divide? Many cancer cell lines have existed for decades and do not show a tendency to decrease in their activity. Of course, cancer cells undergo simplification.

Cancer cells have various mechanisms to bypass this limit. These cells have a more active metabolism than healthy cells. Frequent division leads to the fact that they have to constantly recreate their elements, as they are distributed among the daughter cells.

Therefore, they always have young proteins that have a higher potential than older ones. The cage therefore practically does not wear out. The question arises, what if we try to overcome the Hayflick limit for healthy cells? It turned out that this task is not absolutely fantastic. It turned out that there is such an enzyme telomerase. Its task is to increase the telomeres of chromosomes; it is inactive only in differentiated (specialized) cells.

What if you try to activate it? For a long time, everything rested on the fact that differentiated cells with active telomerase acquired the features of cancer cells. As a result of the research, it was possible to change telomerase in such a way that cells with working telomerase had normal properties.

On the one hand, if we overcome the Hayflick limit, then we can get enough of some types of differentiated cells. But this limit is set by nature, so to speak, with a protective purpose. If a cell gets out of control for some reason, and the body fails to kill it or force it to commit suicide (apoptosis), then it will divide for a long time, oppressing neighboring normal cells, as in the case of cancer. Therefore, you need to go down this path very carefully.

Introduction

The problem of aging of the body and prolongation of human life is one of the most important topics that interested almost any human civilization. The study of the mechanisms of aging of the human body remains an extremely urgent problem at the present time. Let us point out only one demographic indicator: by the beginning of the 21st century, in developed countries, the share of the population aged 65 years and over is 10-14%. According to available forecasts, this figure will double in 20 years. Population aging poses many unsolved problems for modern medicine, including the task of extending life in a state of active old age for a significant period of time. It is impossible to solve this grandiose problem without having an idea about the mechanisms of aging of the body. We will focus only on the discussion of the mechanisms of cell aging, and those of them that are genetically determined, that is, inherent in the human body from birth to death.

Hayflick limit

In 1961, the American cytologist Leonard Hayflick, together with another scientist P. Moorhead, conducted experiments on the cultivation of human embryonic fibroblasts. These researchers placed individual cells in a nutrient medium (before incubation, the tissue was treated with trypsin, due to which the tissue dissociated into individual cells). In addition, L. Hayflick and P. Moorhead used a solution of amino acids, salts, and some other low molecular weight components as a nutrient medium.

Fibroblast division began in the tissue culture, and when the cell layer reached a certain size, it was divided in half, again treated with trypsin, and transferred to a new vessel. These passages continued until cell division ceased. Regularly this phenomenon occurred after 50 divisions. Cells that stopped dividing died after a while. The experiments of L. Hayflick and P. Moorhead were repeated many times in various laboratories in many countries of the world. In all cases, the result was the same: dividing cells (and not only fibroblasts, but also other somatic cells) stopped dividing after 50-60 passages. The critical number of somatic cell divisions is called the Hayflick limit. Interestingly, for somatic cells of different vertebrate species, the Hayflick limit turned out to be different and correlated with the lifespan of these organisms.

They die after about 50 divisions and show signs of aging as they approach this limit.

This boundary has been found in cultures of all fully differentiated cells, both in humans and in other multicellular organisms. The maximum number of divisions varies depending on the type of cell and varies even more depending on the organism. For most human cells, the Hayflick limit is 52 divisions.

The Hayflick boundary is associated with a reduction in the size of telomeres, the stretches of DNA at the ends of chromosomes. If the cell does not have active telomerase, as most somatic cells do, the size of the telomeres decreases with each cell division because DNA polymerase is unable to replicate the ends of the DNA molecule. However, due to this phenomenon, telomeres should shorten very slowly - by several (3-6) nucleotides per cell cycle, that is, for the number of divisions corresponding to the Hayflick limit, they will shorten by only 150-300 nucleotides. Currently, an epigenetic theory of aging has been proposed, which explains telomere erosion primarily by the activity of cellular recombinases that are activated in response to DNA damage caused mainly by age-related derepression of mobile genome elements. When, after a certain number of divisions, telomeres disappear completely, the cell freezes at a certain stage of the cell cycle or starts a program of apoptosis, a phenomenon of smooth cell destruction discovered in the second half of the 20th century, which manifests itself in a decrease in cell size and minimization of the amount of substance entering the intercellular space after its destruction.

Notes

Since the Nobel Prize was awarded in 2009 for the discovery of how chromosomes are protected by telomeres, laboratories around the world have begun offering telomere length measurements to determine "biological age". For example, in one of the institutions in Moscow, this analysis will cost the client 18,000 rubles. What is the essence of this discovery, does the length of telomeres affect the life expectancy of a person and is it worth spending money on this examination - this is my article today.

Hayflick limit

In 1961, Leonard Hayflick, observing the cultivation of human fibroblasts, discovered the death of the culture after 50 divisions. Cells could be transferred from medium to medium, frozen for any period, but even after thawing they somehow “remembered” how many divisions had already taken place and divided as many times as there were left up to 50. The phenomenon named after the scientist - the Hayflick limit - remained for years inexplicable, but even then they started talking about the life expectancy of a person programmed in the genes.

It was only in 1971 that Aleksey Olovnikov noticed that the Hayflick limit is characteristic of cells with DNA that is not closed in a ring, while bacteria with circular DNA multiply without restrictions. The scientist put forward a hypothesis marginotomy, which suggested that the limit of cell division with linear DNA is due to incomplete copying of the terminal sections of the chromosome at the time of cell division. Olovnikov's idea is ingenious and at the same time simple, it is easy to explain it even to a schoolboy. I will try to talk about this in the context of evolutionary theory.

As the cell prepares to divide, the DNA polymerase enzyme travels along the chromosome to make a copy of it. If the chromosome has a circular structure, the enzyme successfully completes the full circle, and the ends of the copy stick together to form a chromosome for a new cell.

In the era of unicellular organisms, chromosomes had a ring structure. But sometimes, as a result of mutations, it happened that the ends of the new chromosome did not stick together to form a ring, and the DNA strand remained open. This is how bacteria with linear chromosomes appeared. A bacterium that received such a chromosome faced a copying problem when it was its turn to divide. The polymerase, having reached the end of the linear chromosome, stops and cannot copy the terminal region approximately equal to the enzyme's own length.

This idea dawned on Olovnikov when he went down the subway after a lecture on Hayflick's experiments at Moscow State University. He reasoned: "what happens to the polymerase on linear chromosomes is analogous to how the second car of the train will never reach a dead end and stop at a distance equal to the length of the locomotive." But let's go back to evolutionary theory to understand how nature solved the problem of bacteria with linear chromosomes.

The propensity to form linear chromosomes could be inherited by daughter cells, and with each generation the genome of daughter bacteria was shortened. As soon as a gene vital for a bacterium turned out to be undercopied, the colony stopped growing and died. Therefore, at first, bacteria with linear chromosomes were quickly weeded out as a result of natural selection.

However, some of these bacteria, as a result of accidental viral insertions, received additional ends on the chromosomes, which served as a kind of reserve - these terminal sections of the chromosome could be shortened with each division without threatening important genes. Olovnikov, assuming the presence of these regions at the ends of linear human chromosomes, called them telogens(modern name - telomeres).

Ok, but sooner or later, telomeres will be used up after 50-100-200 divisions, and the death of a colony of bacteria with linear chromosomes seems inevitable. Moreover, linear chromosomes are the only variant of DNA organization for all existing multicellular organisms, including humans. Why did seemingly defective linear chromosomes end up in highly developed organisms? Presumably, for the first multicellular organisms, the ability to divide indefinitely turned out to be harmful. Just imagine your cells doubling unhindered, turning your beautiful body into embryonic biomass. But the first multicellular organisms did not have immune and hormonal systems and other mechanisms regulating cell division. Perhaps that is why natural selection favored multicellular organisms that arose from unicellular organisms with linear chromosomes.

So, telomeres are finite, and nature requires procreation. How to explain the formation of the human body into trillions of cells from one zygote without shortening the telomeres? To resolve this contradiction, the ingenious Olovnikov predicted that telomeres are able to build up a special enzyme, which he gave the name tandem polymerase(modern name - telomerase). Many years later, American scientists experimentally confirmed Olovnikov's guesses and proved that telomerase is able to attach to the end of the chromosome and, acting as a matrix, increase telomeres, for which they received the Nobel Prize in 2009.

Hayflick limit in humans

In modern animal and human organisms, the problem of the Hayflick limit is not so relevant - so far it has not been possible to establish a relationship between telomere length and life expectancy. Therefore, do not rush to pay money for the study of telomere length. In addition, this mechanism of limiting cell division is unlikely to stop cancer. Both stem and cancer cells easily increase the telomeres of their chromosomes by increasing the activity of telomerase. A good example is a cell culture obtained 60 years ago from a tumor of the cervix of an American Henrietta Lacks. Its cells are still used in laboratories all over the world, they flew into space and were blown up by an atomic bomb, they were used to develop vaccines and cures for cancer, and this year they even made a feature film about them. The famous HeLa cells (from He nrietta La cks) survived the woman herself and her children, and in terms of their biomass many times outgrew the mass of all of them combined. Thus, telomerase easily solves the problem of the Hayflick limit.

In addition, the ability of stem cells to asymmetric division not only solves the problem of the Hayflick limit without the participation of telomerase, but also the problem of accumulation of mutations, the frequency of which increases with each cell division. New data on stem cell division create prerequisites for the potential immortality of not only individual cells, but the whole organism.

Asymmetric division - the potential for immortality

It is logical that the division of one cell ends with the formation of two daughter cells, one of which contains the original chromosome, and the second gets its copy. Even if we are talking about the division of a cell with a ring chromosome, then the daughter cells are not equivalent to each other, since in the process of copying DNA, errors inevitably occur that go to the daughter cell that received a copy of the chromosome. If we talk about cell division with a linear chromosome, then the daughter cell that received a copy not only contains more mutations, but also receives shortened telomeres. Thus, it can be assumed that after many cycles of stem cell divisions in the body there will be one cell with the original chromosome, and all the others will contain shortened copies with mutations.

Taking into account that after several cycles of divisions there is a gradual maturation (differentiation) of cells, sooner or later the cell with the original chromosome, like all cells of its generation, having fulfilled its function, will die, as billions of blood cells, skin or intestinal epithelium die every day. In this situation, we are forced to admit that all the original stem cells stored in our body in the womb are used up and mutations inevitably accumulate with age, and telomeres inevitably shorten. This is how the inevitable decrepitude and mortality of our body was explained for a long time.

However, in 1975, the asymmetric division hypothesis was put forward, suggesting that the division of a stem cell ends with the formation of not two daughter cells, but one, while the second cell remains a stem cell. In 2010, it was experimentally confirmed that the process of distribution of the original chromosome and its copy is asymmetric. It turned out that the original chromosomes remain in the stem cell, which retains its stemness, and the copies end up in the daughter cell, which forms a colony of progressively differentiating cells with a limited lifespan.

In this scenario, stem cells have a literally inexhaustible potential for self-sustaining:

1. They preserve the original DNA without accumulating mutations and without the risk of being left without telomeres;
2. Rarely divide, synthesize proteins little and are metabolically weakly active, which means that it is easier for other cells to survive the lack of oxygen and nutrition, intoxication and radiation;
3. They do not differentiate into mature cells and are not consumed during life.

Conclusion

In my laboratory, I grow these giant colonies of blood cells in just 10 days. Each red spot is thousands of young red blood cells formed from a single stem cell. It is possible that the ancestor of the colony is somewhere among them and is ready to form more than one such colony - it is enough to change the concentration of hormone-like division stimulators.

Approximately this happens in the bone marrow of each of us throughout life. Most mature blood cells live from minutes to months, so billions of blood cells need to be renewed every day.

But why do the processes of renewal of blood and other tissues of the body slow down with age? I adhere to the version that stem cells remain viable throughout our lives. And the slowdown in regeneration processes is due to the "bricking up" of stem cells by connective tissues, as a result of which they cease to receive signals from the macroorganism about the need for renewal.

About why this happens - I'll tell you sometime next time. In order not to miss updates - ! And if you do not have a LiveJournal account, subscribe to updates in