Zombie cells are behind aging: this is how scientists aim to eradicate them

Time leaves its mark on our bodies, and one of the main culprits is the so-called “senescent cell”, also known as zombie cells. And as the name implies, since these cells have stopped dividing, they never die, but instead accumulate in tissues and release inflammatory substances that contribute to aging and various diseases.

in our body Logically, the body is not stupid, since one of its purposes is to deal with these rebel cells. But the problem we have here is that it cannot eradicate these rebel cells because the ‘cleansing’ process fails over the years.

It is investigated. This year a group of researchers worked on how our body works with these cells, and the heroes here seem to be macrophages, a type of white blood cell that acts as our body’s cleaning crew, engulfing all dead or damaged cells. However, it has been found that as we age, the function of these macrophages declines drastically.

The cause appears to lie in a molecule called prostaglandin E2 and its receptor EP2. This is a signaling pathway that appears to divert the metabolism of macrophages, since instead of using glucose as energy to consume zombie cells, this signal causes them to store glucose in the form of glycogen, leaving them without the energy they need to perform their functions.

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precedent Already in 2021 there was a research team that showed that blocking this pathway restored memories in old mice. But this new study goes further and shows that, in old mice, reducing EP2 signaling in resident macrophages not only improved their ability to eliminate these zombie cells, but also prevented cognitive decline, weakness, loss of muscle mass or general inflammation.

In addition, the researchers tested pharmacological inhibition of EP2 and observed similar changes in tissues of elderly and sick people.

the way forward The relationship between inflammation and age-related diseases is not new, as already in 2001, the Rotterdam Study, published new england, It has been suggested that long-term use of nonsteroidal anti-inflammatory drugs may be associated with a reduced risk of Alzheimer’s disease. However, it is important to note that the subsequent randomized ADAPT trial did not confirm this protective effect, underscoring the complexity of translating this system to humans.

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the future The idea of ​​eliminating zombie cells as an anti-aging therapy gained momentum with several research works, which showed in mice that eliminating senescent cells delayed aging-related disorders and extended healthy lifespans.

Now, the good news on our table is that these investigations of anti-aging therapies, including senolytics, are at an important transition stage toward clinical trials. But the challenge on our table is to translate these promising laboratory discoveries into safe and effective therapies for humans, aiming not just to live longer, but to live better, free from the chronic diseases of aging.

Picture | Kimono!

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