By Dr. Asnat Raziel, bariatric surgeon specializing in obesity treatment, metabolic health and healthy longevity; Director of the Multidisciplinary Center for Obesity Treatment, Assia Medical, Assuta Ramat HaChayal, Tel Aviv
Zombie cells: what the study found
Zombie cells are among the prime suspects in the aging process. A new study explains why they build up with age. First, the cells’ “cleanup” system weakens. Second, immune cells struggle to clear them away. However, the researchers found a way to restore this clearance capacity in mice, which makes it a promising new treatment target.
The study was carried out by researchers at the Albert Einstein College of Medicine in New York, led by Prof. Ana Maria Cuervo, and published in the journal Nature Aging.
What are zombie cells (senescent cells)?
Zombie cells, known in scientific terms as senescent cells, are old cells that have stopped dividing. Yet they don’t die; they stay in the tissue. In fact, they release pro-inflammatory substances into their surroundings. That’s why their buildup is linked to many age-related diseases and to faster aging.
Interestingly, in small numbers they can even be helpful, for example in wound healing. But as they accumulate with age, they promote inflammation, fibrosis and cancer.
Why the clearance system fails
In a young body, immune cells called macrophages “swallow” old cells. To do this, they rely on a cellular recycling mechanism called CMA (chaperone-mediated autophagy). With age, CMA activity declines. As a result, senescent cells change what they secrete, and they also suppress CMA in the macrophages themselves. This creates a vicious cycle in which clearance fails and the cells keep accumulating.
Restoring the cleanup: activating autophagy (CMA)
Here comes the encouraging part. The researchers activated the CMA mechanism with a drug. As a result, the burden of senescent cells in old mice went down. What’s more, the severity of pulmonary fibrosis in a mouse model was reduced. In other words, renewing the cleanup system may help aging tissues.
Zombie cells and wound healing: what the mice showed
Mice whose immune cells lacked the CMA mechanism healed wounds much more slowly. They also accumulated a large number of old cells around the wound. On the other hand, a drug that reactivated the mechanism lowered markers of aging. The effect, however, varied between tissues and between males and females. Timing also turned out to be critical to success.
Zombie cells and longevity
This approach complements the field of senolytics. Until now, most of the effort has focused on killing the old cells. Now a new idea is joining it: restoring the body’s natural clearance system. This is an important direction in longevity medicine. It joins other tools being studied today, as described in my article on biohacking, NAD+ and peptides, and ties in with measuring the pace of aging using biological clocks.
What still needs to be tested?
First, most of the evidence comes from mice and from cells in a dish, so it has to be confirmed in humans. Second, the effect was not uniform across tissues or between the sexes. The next step, therefore, is to find out whether this can be turned into a safe treatment.
The bottom line
The research on zombie cells points to an interesting new drug target. For now, though, the work has been done only in mice and cells, so it will take a long time before it can be applied in people. Ultimately, understanding the cell’s cleanup mechanisms and the science of aging may change the way we treat aging. Please note: the information in this article is general only and is not a substitute for personal medical advice.
Sources
Decline of chaperone-mediated autophagy in aging impairs macrophage clearance of senescent cells
Restoring cellular recycling helps the body clear harmful zombie cells
