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The miracle of DNA repair: How do cells repair themselves when they are damaged?
In the microscopic world of life, DNA is the blueprint that carries genetic information. However, this sophisticated structure is not static. Over time or due to external environmental influences, DNA faces various types of damage that may threaten the normal function of cells. So how exactly do cells repair themselves when they encounter this damage?
There are many types of DNA damage, including single-strand breaks, missing nucleotides, and changes in chemical structure, all of which may interfere with cell replication and its normal physiological processes.
DNA damage is usually caused by natural processes or external environmental factors. For example, each cell in the human body generates up to 10,000 oxidative damages per day, which, if not repaired, accumulate and contribute to aging and other health problems. This leads to the DNA damage response (DDR), a complex signaling mechanism that detects DNA damage and initiates appropriate repair mechanisms.
Repaired DNA can continue to allow cells to divide normally, but if the damage is too severe, the cell may initiate apoptosis to protect itself.
During the cell cycle, cells pass through specific checkpoints to ensure they are healthy before entering mitosis. Especially during the synthesis phase (S phase), cells are most sensitive to DNA damage. From the G1 checkpoint to the G2 checkpoint, the cell carefully checks the integrity of the DNA to avoid creating more damage during replication.
The repair mechanisms triggered by DNA damage can be mainly divided into the following categories: base excision repair, nucleotide excision repair, homologous recombination repair, etc. Each repair pathway has its own specific role and repair accuracy. For example, base excision repair can repair oxidative damage without causing other damage, while nucleotide excision repair targets larger and more complex DNA lesions.
As we age, our cells' ability to repair themselves becomes less effective, which is why we tend to accumulate more DNA damage as we age. The study showed that in various tissues of mice, the steady-state levels of DNA damage were significantly increased compared to young cells, indicating the accumulation of DNA damage with age.
The risk of DNA damage is greatly increased under long-term chronic inflammation or environmental influences such as alcoholism. These factors not only threaten the health of cells, but may also lead to the occurrence of cancer.
Environmental damage to DNA, such as exposure to ultraviolet light or certain chemicals, tends to result in more severe double-strand breaks. This type of damage not only affects the function of a single cell, but long-term accumulation may also affect the entire cell population and even cause tissue aging and pathology. Cell repair is the key, but like a double-edged sword, mistakes in the repair process can easily lead to mutations and ultimately cancer.
Compared to homologous recombination repair, non-homologous end joining repair is another way to deal with double-strand breaks. Although it has fast processing speed, its accuracy is somewhat lacking. Therefore, cells that use this repair method may face the risk of extinction if they suffer other DNA damage at the same time. This situation reflects the fragility of cells' self-repair ability.
In cancer research, excessive amounts of DNA damage often enable cancer cells to proliferate, so understanding this process is critical to finding new treatments.
In addition, studies have also shown that the occurrence of oxidative damage is closely related to the formation of memory in the brain. Oxidative DNA damage can affect the expression of certain genes in neurons, which are turned on or off during memory formation. Therefore, DNA damage is not only a threat to health, but may also affect learning and memory functions.
In this seemingly small but far-reaching repair process, scientists are constantly exploring how cells recognize, respond to and repair DNA damage. With further research in the future, we may be able to better understand this extremely important life process and provide new ideas for treatments for anti-aging, anti-cancer and brain health. As a result, DNA damage and repair have once again become the focus of continued exploration in the scientific community. However, we cannot help but ask, how much can the potential of DNA repair mechanisms help us overcome the challenges of health and aging?
