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This study found that hair follicle stem cells in the hairpoor mouse, a model for Marie-Unna hypotrichosis, lose their quiescent state, leading to a disordered hair cycle and contributing to alopecia.

In this study, researchers found that mice lacking the transcription factor FOXC1 in their hair follicle stem cells had increased rounds of hair regeneration but experienced hair thinning due to impaired ability to maintain stem cell quiescence and adhesion.

In this study, researchers found that Hdac1 and Hdac2 are crucial for maintaining the quiescence and survival of dermal papilla cells in the hair follicle, regulating the hair cycle by controlling cell-cycle genes and Wnt signaling.

This study found that the dermal papilla of the hair follicle regulates stem cell quiescence and regeneration by modulating Shh and Wnt signaling pathways, highlighting the importance of signaling cross talk in regeneration.

This study found that in hairpoor mice, disruptions in hair follicle stem cell quiescence and signaling pathways lead to disturbed hair cycles, which may help explain alopecia development in Marie-Unna Hypotrichosis patients.