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This study found that immune-mediated destruction of bulge stem cells is a key factor in the alopecia observed in AE mice, suggesting it as a model for studying primary cicatricial alopecias, particularly lichen planopilaris.

This study found that the Gsdma3 gene is necessary for normal hair follicle differentiation in mice, with its mutation leading to progressive hair loss and defects in hair structure.

This study found that Gsdma3 mutations in mice led to thicker skin and longer hair infundibula, possibly by negatively regulating β-catenin expression in the epidermis.

This study demonstrated that dominant mutations in mouse gasdermin A3 disrupt mitochondrial oxidative stress regulation, suggesting a gain-of-function effect on epidermal differentiation.

This study found that Gsdma3 mutation in mice allows hair follicles to bypass a typical telogen phase and directly enter the anagen phase, suggesting Gsdma3's role in hair cycle transitions by regulating Wnt signaling.