Aging reprograms skin genetic activity and promotes inflammation, study reveals
As we age, the skin loses part of its ability to regenerate, heal wounds and maintain an effective barrier against the outside world. Among the causes of this deterioration is low-grade, persistent age-associated inflammation, but the mechanisms that keep this response active in skin cells are not yet well understood.
As we age, skin loses its ability to regenerate and maintain a protective barrier against the outside world. One factor contributing to this deterioration is persistent, low-grade inflammation in skin cells. Researchers led by Drs. Guiomar Solanas and Salvador Aznar Benitah have discovered a molecular mechanism that explains this process.
During aging, two proteins - BMAL1 and YAP - change how they interact and increase activity of inflammatory genes in the epidermis, the outermost layer of skin. The study, published in Nature Aging, shows that this inflammatory shift happens independently of the body's daily rhythms. Both proteins normally maintain skin cell health and identity, but with age, skin stiffness and increased inflammatory signals cause them to concentrate in regions of DNA that activate inflammatory genes.
The findings build on a 2023 study that identified IL-17 as a key inflammatory signal in skin aging. Blocking this protein in aged mice reduced persistent inflammation and delayed skin aging features. While the research clarifies how aging and inflammation are connected in the skin, the next step is to explore if this mechanism can be safely regulated without compromising essential skin functions.
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