Succinylated Type\nI Collagen Regulates Ferroptosis\nto Attenuate Skin Photoaging

During the process of photoaging in the skin, Succinylated\ntype\nI collagen has a significant effect on reversing the damage caused\nby UVB radiation, with the regulation of cellular ferroptosis being\none of its important pathophysiological mechanisms. Specifically,\nSuccinylated type I collagen reduces the expression of key cell cycle\nregulators P16, P21, and P53, as well as the ferroptosis-related factor\nAcyl-CoA Synthetase Long Chain Family Member 4 (ACSL4), induced by\nUVB radiation in cells and tissues. Meanwhile, it increases the expression\nof key factors Glutathione Peroxidase 4 (GPX4) and Solute Carrier\nFamily 7 Member 11 (SLC7A11), which inhibit ferroptosis. Additionally,\nour study also reveals the impact of Succinylated type I collagen\non the levels of malondialdehyde (MDA), glutathione (GSH), and reactive\noxygen species (ROS) in cells and tissues, directly affecting the\ncells’ ability to cope with oxidative stress. This further\nsuggests that Succinylated type I collagen may improve skin photoaging\nthrough various pathways, including regulating ferroptosis, antioxidation,\npromoting collagen synthesis, protecting the skin barrier, reducing\npigmentation, and inhibiting inflammatory responses, contributing\nto maintaining healthy and youthful skin.