Skin inflammation in aging tied to a shifted protein pair

In healthy skin, two proteins work together: BMAL1 and YAP. BMAL1 is a component of the cell’s biological clock, the internal timing system that regulates day-night rhythms. YAP responds to mechanical signals from the cell’s environment. Together, they keep skin cells stable and in balance.

The researchers, publishing in Nature Aging, found that this cooperation changes with age. The joint activity of BMAL1 and YAP shifts toward regions of DNA that drive inflammatory responses, partly triggered by age-related changes in the cellular environment. The result is that skin tissue produces more inflammatory signals on a structural basis, even without external cause.

The biological clock takes on an unexpected role

Notably, BMAL1 here is not acting as a clock gene in the traditional sense. Normally it regulates the timing of cellular processes. In aged skin it still does that, but it also cooperates in activating inflammatory genes. This is a different role than previously assumed for this protein.

Chronic low-grade inflammation in older tissue, known as inflammaging (a combination of ‘inflammation’ and ‘aging’), is a widely studied phenomenon. It refers to persistent low levels of inflammation in the body not caused by infection. In longevity research, inflammaging is considered a potential contributor to multiple age-related conditions, though the scale of that contribution varies by tissue and individual.

What this means for skin aging

This study provides a concrete target for future research: the BMAL1-YAP cooperation as a potential point of intervention. The researchers note these are preliminary findings. Whether interventions targeting this mechanism would be effective or feasible in people remains unclear. No clinical applications exist yet.

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