Department of Pathophysiology, Guangdong Medical University, Dongguan 523808, China.
School of Public Health, Guangdong Medical University, Dongguan 523808, China.
ACS Appl Mater Interfaces. 2024 Oct 23;16(42):56744-56761. doi: 10.1021/acsami.4c11952. Epub 2024 Oct 11.
During the process of photoaging in the skin, Succinylated type I collagen has a significant effect on reversing the damage caused by UVB radiation, with the regulation of cellular ferroptosis being one of its important pathophysiological mechanisms. Specifically, Succinylated type I collagen reduces the expression of key cell cycle regulators P16, P21, and P53, as well as the ferroptosis-related factor Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4), induced by UVB radiation in cells and tissues. Meanwhile, it increases the expression of key factors Glutathione Peroxidase 4 (GPX4) and Solute Carrier Family 7 Member 11 (SLC7A11), which inhibit ferroptosis. Additionally, our study also reveals the impact of Succinylated type I collagen on the levels of malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) in cells and tissues, directly affecting the cells' ability to cope with oxidative stress. This further suggests that Succinylated type I collagen may improve skin photoaging through various pathways, including regulating ferroptosis, antioxidation, promoting collagen synthesis, protecting the skin barrier, reducing pigmentation, and inhibiting inflammatory responses, contributing to maintaining healthy and youthful skin.
在皮肤光老化过程中，琥珀酰化 I 型胶原对逆转 UVB 辐射引起的损伤具有显著作用，其细胞铁死亡调节是重要的病理生理学机制之一。具体而言，琥珀酰化 I 型胶原降低了 UVB 辐射诱导的细胞和组织中关键细胞周期调节剂 P16、P21 和 P53 以及铁死亡相关因子酰基辅酶 A 合成酶长链家族成员 4（ACSL4）的表达。同时，它增加了谷胱甘肽过氧化物酶 4 (GPX4) 和溶质载体家族 7 成员 11 (SLC7A11) 的关键因子表达，抑制铁死亡。此外，我们的研究还揭示了琥珀酰化 I 型胶原对细胞和组织中丙二醛 (MDA)、谷胱甘肽 (GSH) 和活性氧 (ROS) 水平的影响，直接影响细胞应对氧化应激的能力。这进一步表明，琥珀酰化 I 型胶原可能通过多种途径改善皮肤光老化，包括调节铁死亡、抗氧化、促进胶原蛋白合成、保护皮肤屏障、减少色素沉着和抑制炎症反应，有助于维持健康年轻的皮肤。
