Clearing aging cells from the skin helped older mice heal wounds faster, suggesting a new approach to wound repair.

Published in Aging (Aging-US), the study examined ABT-263, a senolytic drug. Senolytic drugs are designed to remove senescent cells, which are damaged or stressed cells that stop dividing but remain alive.

As people age, senescent cells can accumulate in tissues and affect repair. Researchers wanted to see whether removing these cells from aging skin could improve the skin’s ability to heal.

The researchers applied ABT-263 directly to the skin of aged mice for five days. The treatment reduced signs of cellular senescence. The mice were then given small skin wounds. By day 24, 80% of mice treated with ABT-263 had completely healed wounds, compared with 56% of untreated aged mice.

The treatment also temporarily increased inflammatory activity in the skin. Although prolonged inflammation can delay healing, an inflammatory response is an important early part of normal wound repair. This response may have helped activate repair processes.

ABT-263 also increased activity in genes involved in tissue rebuilding, including those linked to collagen production and new blood vessel formation. Collagen provides structural strength to skin, while new blood vessels supply healing tissue with oxygen and nutrients.

Treatment mainly affected older skin, which contained more senescent cells. Applying the drug directly to the skin may also limit exposure to other parts of the body.

The findings raise the possibility of using topical senolytic treatment before injury to improve healing after surgery or in chronic wounds in older people. However, the research has so far been conducted only in mice. Human studies are needed to determine whether topical ABT-263 is safe and effective and whether the same benefits occur in people with age-related delayed healing.

REFERENCE: L Maria Shvedova, et al.; Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing. Aging, 2024; 17 (1): 16 DOI: 10.18632/aging.206165

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Article Source : Aging

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