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Getting the latest healthcare news for you
Aging skin has a chronic inflammation problem, and researchers just figured out why. A new study in Nature Aging reveals that two proteins — BMAL1 and YAP — team up in older skin to ramp up inflammatory gene activity. The culprit? A signal called IL-17, sent by immune cells, that hijacks this protein duo and keeps inflammation burning.
Aging skin has a chronic inflammation problem, and researchers just figured out a key reason why. A new study published in Nature Aging, led by scientists at IRB Barcelona, identifies a molecular mechanism in which two proteins — BMAL1 (known for its role in the circadian clock) and YAP (which helps cells respond to physical stress) — change how they work together as skin ages. Instead of maintaining normal skin function, they begin amplifying inflammatory gene activity in the epidermis.
The trigger? A signaling molecule called IL-17, released by immune cells in the deeper layer of the skin. As skin stiffens with age and inflammatory signals rise, IL-17 activates YAP, which then teams up with BMAL1 to drive inflammation further. When researchers blocked IL-17 in aged mice, YAP activity and inflammatory gene expression both dropped — building on a 2023 finding from the same lab that first flagged IL-17 as a key player in skin aging.
Key Takeaways:
Why it matters: Chronic low-grade inflammation in aging skin contributes to poor wound healing, barrier breakdown, and skin disease. Pinpointing this BMAL1-YAP-IL-17 axis opens a potential therapeutic window, though researchers caution that any intervention must avoid disrupting the skin's essential protective functions.
