Stopping cell division during aging depends on a single protein

Scientists have established that ATM protein, which reacts to DNA breaks and usually protects genetic material from damage, is fully responsible for triggering this mechanism. If the ATM is blocked, the cells continue to divide longer than normal. Moreover, if you turn off the ATM in cells that are already old, they start dividing again — that is, the stop turns out to be reversible.

The researchers also explained a mystery that biologists have been facing for decades: cells in laboratories where oxygen levels are higher age faster than in the body. It turned out that with a high oxygen content, ATM becomes overactive: it begins to perceive shortened telomeres too strictly as dangerous damage and prematurely activates the mechanism for stopping division. In a living organism, where there is significantly less oxygen, ATM works more smoothly, and cells retain their ability to divide longer.

Experiments have shown that the ATM’s reaction to reactive oxygen species, which change its structure, plays a key role in this. When oxygen levels are low, ATM is less sensitive, and cells tolerate shorter telomeres. At high levels, the protein reacts too quickly, and aging occurs earlier.

The data helps to better understand how cancer protection programs work: most tumors develop in low-oxygen environments where ATM is partially suppressed. This allows cancer cells to continue dividing, even when their telomeres are critically short. In the future, restoring ATM activity in tumors may be a strategy that forces cancer cells to stop.

The researchers emphasize that their work is changing the approach to studying cell aging in the laboratory. Many conclusions drawn when working with cells in high oxygen conditions may work differently in physiological conditions. Now it is important to check the results in conditions closer to reality.

The discovery of ATM’s role as the sole regulator of replicative aging is an important step towards understanding how cells protect the body from cancer and what exactly triggers their biological aging.