Boosting Gene ZNF865 With CRISPR Reversed Aging Signs in Degenerated Spinal Disc Cells

The work was published in Aging Cell in 2026. It is laboratory research: human and mouse disc tissue samples, human disc cells grown in the lab, and an experiment in living animals. It is not a trial in people.

The gene is called ZNF865. It was only recently identified as a protein that regulates many genes involved in protein processing, cell senescence and DNA damage repair. Senescent cells have stopped dividing but stay in the tissue. They release signals, known as the SASP, that can harm their surroundings. The authors note that senescence contributes to age-related diseases, including degenerative disc disease. How senescence is controlled in the discs is still poorly understood.

The team reports that ZNF865 levels fall with age and with disease in both human and mouse disc samples. The authors used CRISPR, a gene-editing tool, to turn the gene's activity up or down. Lowering it in disc cells from people without symptoms pushed those cells into senescence. That suggests the gene is needed for healthy cell function.

Raising it had the opposite effect. In degenerated cells from the disc's soft center, called the nucleus pulposus, restoring ZNF865 reduced senescence, SASP signals and DNA damage. It also increased the cells' production of the extracellular matrix, the material that gives tissue its structure. In addition, it returned chromatin accessibility and gene expression to a healthy state. Chromatin accessibility describes how open the DNA is to being read by the cell.

The living-animal test went one way only. Using CRISPR to turn down ZNF865 caused disc degeneration and painful behaviors. The coverage by Lifespan.io adds that this was done in rats, by injecting ZNF865-silenced disc cells into their spines, and that signs of degeneration appeared in under two months. The same coverage reports that silencing the gene in healthy human cells raised senescence markers roughly fivefold. It also reports that boosting the gene cut differences in chromatin accessibility from healthy cells by 94%. Those figures come from the press article.

Several limits apply. The animal work showed that losing ZNF865 can bring on degeneration and pain. It did not show that adding it back fixes a damaged disc in a living body. Lifespan.io also notes that the human cells came from a limited number of donors and that the gene's molecular mechanism is not yet known. It adds that no drugs, antibodies or other tools beyond CRISPR are known to act on ZNF865 directly. The authors call the gene a potential therapeutic target, which is a cautious description.

For anyone with back pain today, nothing changes. This is not a treatment, and it is not a sign that gene editing for backs is close. The finding does point to a possible driver of disc aging: loss of a gene that helps cells cope with DNA damage and avoid senescence.

The next step to watch is a test of whether raising ZNF865 in a living animal can slow or reverse disc degeneration.

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