Scientists identify three distinct types of ‘senescent’ skin cells, opening the door to more precise therapies.
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Your body is teeming with microscopic zombies. Known as senescent cells, these are cells that have stopped dividing but refuse to die.
In the skin, some of them speed up aging and inflammation, while others help heal wounds.
Now, researchers have found that these zombie cells aren’t all the same—and that difference may be the key to targeting the harmful ones without wiping out the helpful.
Not all zombie cells are created equal
In a new study published in Science Advances, researchers at Johns Hopkins University identified three distinct subtypes of senescent skin cells.
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While all are technically “zombie” cells, only one was closely linked to age.
We’re finding that when a skin cell goes into senescence, or a zombie-like state, the cell could go down one of three different paths, each leading to a slightly different subtype,
said biomedical engineer Jude Phillip, co-author of the study.
To map the differences, the team collected fibroblasts—structural skin cells—from healthy donors aged 20 to 90.
They artificially aged them in the lab, then used machine learning to analyze the cells’ physical features and biomarkers. Of the 11 types of cells they observed, three stood out as definitively senescent, labeled C7, C10, and C11, as reported by Popular Science.
Better drugs, better outcomes
The team tested how each subtype responded to drugs currently in trials for targeting senescent cells. One of the most advanced, a combo of dasatinib and quercetin, effectively cleared subtype C7—but was less effective against C10, the type more common in older individuals.
That insight could be critical in diseases where senescent cells cause harm, including dementia, diabetes, and cardiovascular disease. If researchers can eliminate only the bad actors, they could prevent the collateral damage of destroying beneficial cells.
Jude Phillip explains:
With our new findings, we have the tools ready to develop new drugs or therapies that preferentially target the senescence subtype that drives inflammation and disease,
Implications for cancer care
Senescence is already a focus in cancer research, where some therapies aim to force malignant cells into a non-dividing zombie state. But that strategy has a catch: if those senescent cells aren’t cleared, they may linger and do damage.
Chemo drugs themselves can also leave behind zombie fibroblasts, potentially making recovery harder. With the ability to tell harmful senescent cells apart from neutral or helpful ones, new “senotherapies” could sweep away the bad while leaving the good intact.
As Phillip put it:
Eventually, the dream is to be able to provide more information in a clinical setting to help with individual diagnoses and boost health outcomes.