British Journal of Dermatology editor-in-chief proposes using skin to test treatments for aging
British Journal of Dermatology editor-in-chief proposes using skin to test treatments for aging
In an article published on 26 October 2026, John McGrath proposed collecting skin samples repeatedly to track changes in senescent cells and DNA. He also calls for the same trials to assess wound healing and the skin’s protective function.
For decades, the effects of anti-aging skin treatments have been assessed using photographs and wrinkles, McGrath writes in an editorial. A damaged cell can permanently stop dividing while remaining metabolically active. As these senescent cells accumulate in the skin, they release substances that sustain inflammation and break down collagen and elastin, the proteins that give skin its strength and elasticity. The skin becomes thinner and less able to protect the body.
In a Mayo Clinic experiment, senescent fibroblasts, a type of connective tissue cell, were transplanted into the skin of young mice. A control group received dividing fibroblasts. After several months, mice that received senescent cells showed increased signs of cellular senescence in skin distant from the transplant site and in a brain region involved in memory. These animals performed worse than controls on tests of memory and coordination. McGrath proposes a hypothesis: “The skin may export its aging.”
Senolytics are drugs that eliminate these cells by causing them to die. Applying navitoclax to the skin of old mice reduced the number of cells showing signs of senescence and accelerated subsequent wound closure. Topical application was chosen to limit the drug’s side effects in other tissues. After application, immune cell numbers in the skin increased, as did inflammation. The drug was administered before injury to preserve the senescent cells that appear temporarily during healing and help repair tissue.
Surface skin cells can be collected with adhesive tape for repeated measurements. Mitra Bio developed two skin age “clock” models that estimate age from chemical marks on DNA that change over the years. The models were trained to match these marks to people’s chronological age. In a separate validation set of 75 samples, the predictions differed from actual age by about four years on average. Samples can be collected from the same site on the same person to track changes during treatment.
In an early trial of RLS-1496 cream in patients with eczema, Rubedo reported an average age reduction of 2,1 years according to these clocks. The analysis compared 11 pairs of samples from sun-damaged skin collected before and after four weeks of treatment.
McGrath proposes assessing how changes in cells and DNA marks relate to skin function. Trials should establish how these changes relate to healing and the skin’s ability to retain moisture and protect the body. In McGrath’s assessment, “longevity” products on the market are ahead of the clinical evidence.
Another part of the program is partial reprogramming, in which cells are temporarily induced to produce proteins that alter the activity of their genes. In an experiment in old female mice, a prolonged course of treatment resulted in less scar tissue accumulating in wounds than in control animals. Accumulated DNA mutations remain after reprogramming. In eyelid skin from four people aged 55–73, researchers found mutations associated with cancer development. They estimated that 18–32% of cells in the outer layer of apparently normal, sun-exposed skin carried these mutations. McGrath therefore calls for long-term monitoring for possible tumor development when reprogramming such tissue.