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This article reviews how stem cell exhaustion contributes to aging, emphasizing the balance between proliferation and quiescence as crucial for long-term stem cell maintenance, but it reports no new results.

This study highlights that the mammalian target of rapamycin complex 2 (mTORC2)-Akt signaling axis is essential for hair follicle stem cells to return to their niche and regenerate effectively by regulating metabolic pathways.

In this study, researchers found that the KLHL24-ΔN28 protein variant disrupts hair follicle stem cells in a mouse model, leading to premature hair loss by degrading keratin 15.

This study found that the repressive histone mark H2AK119ub links inhibitory FGF signals with the quiescent state in hair follicle stem cells, revealing a signaling-epigenetic axis crucial for maintaining stem cell quiescence and tissue homeostasis.

In this study, researchers discovered a dominant variant in the ADAM17 gene that causes hypotrichosis with woolly hair, where the mutation leads to hair follicle stem cell exhaustion and abnormal hair follicles, resulting in alopecia.