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This study found that hair loss in an Olmsted syndrome mouse model with a Trpv3 mutation was linked to premature keratinocyte maturation, affecting hair follicle structure and function.

This review discusses current knowledge about the TRPV3 ion channel's role in skin functions and diseases, highlighting its potential as a therapeutic target for pain and itch, though suitable ligands are limited.

In this study, TRPV3G568V mice exhibited periodic hair loss and immune cell infiltration in the dermis, without affecting hair follicle stem cell fate, suggesting a focus on dermal immune cells for future research.

In this study, the researchers introduced a mutation in mice to mimic Olmsted syndrome and found that the mutation caused hair loss due to impaired keratinocyte differentiation and depletion of hair follicle stem cells.

In this study, researchers explored various aspects of the TRPV3 ion channel, including its novel mechanosensitivity to shear stress, and identified novel agonists while investigating how repeated stimulation affects TRPV3 activity, but found no evidence of GPCRs sensitizing the channel.