New GPER1 discovery could revolutionize psoriasis and eczema treatments

A new study published in Cell Death Discovery highlights a potential breakthrough in treating skin inflammation. Researchers have identified G protein-coupled estrogen receptor 1 (GPER1) as a key regulator of keratinocyte growth. This discovery could pave the way for more targeted therapies in conditions like psoriasis and eczema.

The study reveals that activating GPER1 slows down the proliferation of keratinocytes, particularly during the G1 phase of the cell cycle. By interfering with the MAPK/ERK signalling pathway, the receptor reduces levels of pro-inflammatory mediators such as TNF-α and IL-6. This mechanism offers a more selective approach to controlling skin inflammation compared to traditional treatments.

Animal tests further demonstrated the receptor's potential. GPER1 agonists significantly lessened disease severity and histopathological markers in models of psoriasis-like inflammation. The findings also suggest a link between GPER1 and estrogen signalling, providing rapid cellular responses distinct from those triggered by classical nuclear estrogen receptors.

Despite promising preclinical results, no clinical trials for GPER1-targeted therapies in psoriasis or eczema have begun as of March 2026. The study also emphasises the broader role of G protein-coupled receptors (GPCRs) in skin health and disease.

The identification of GPER1's role opens possibilities for developing new topical or systemic treatments. Future research may explore GPER1 agonists as safer alternatives to existing anti-inflammatory drugs. Additionally, measuring GPER1 levels could help tailor therapies to individual patients, improving precision in dermatological care.