Mast cell deficient and neurokinin-1 receptor knockout mice are protected from stress-induced hair growth inhibition

The study demonstrated that both neurokinin-1 receptor knockout mice (NK-1R) and mast cell-deficient mice (W/W) did not experience stress-induced premature catagen phase or hair follicle apoptosis, unlike wild-type mice. This suggests that the interaction between substance P (SP) and mast cell activation through NK-1R is key in regulating hair follicle response to stress. The absence of stress-induced upregulation of SP positive nerve fibers in NK-1R and W/W mice further supports this pathway's role in hair growth regulation. The findings indicate that targeting the SP and NK-1R pathway could be a potential strategy for preventing stress-induced hair loss. Specific numbers of mice and hair follicles analyzed were not mentioned in the summary, but the document indicated a thorough examination across different mice and hair follicles.