Intrinsic ROS Drive Hair Follicle Cycle Progression by Modulating DNA Damage and Repair and Subsequently Hair Follicle Apoptosis and Macrophage Polarization

The study examined the role of intrinsic reactive oxygen species (ROS) in hair follicle cycle progression, focusing on DNA damage, repair, and apoptosis. It found that increased ROS levels during the catagen phase led to DNA damage and activated apoptosis through the AIF-PARP1 and Cytochrome c/Caspase-3 pathways. The research highlighted a seesaw relationship between these pathways, with PARP1 as a key player in DNA repair. Inhibition of PARP1 reduced DNA repair and increased apoptosis, while Caspase-3 inhibition enhanced DNA repair. The study also noted macrophage polarization, with M1 macrophages promoting apoptosis in catagen and M2 macrophages supporting regeneration in anagen and telogen. The findings suggested that ROS and these pathways were crucial for hair cycle regulation, although further research was needed to fully understand these mechanisms.