Photoaging is characterized by chronic inflammation in response to ultraviolet (UV) radiation. UV radiation causes skin cells to produce reactive oxygen species (ROS), which causes oxidative stress and inflammation. ROS can reversibly or irreversibly destroy different cellular compounds, including nucleic acids, proteins, free amino acids, lipids, lipoproteins, carbohydrates, and connective tissue macromolecules. Ferroptosis is a kind of programmed cell death caused by iron dependence and lipid peroxidation and has been recently discovered. Its occurrence is primarily related to iron metabolism, antioxidants, lipid peroxidation, and other processes. In addition, high levels of ROS can trigger oxidative stress, altering the redox balance within cells and thus initiating ferroptosis. Ferroptosis has been implicated in UV-driven skin photoaging. Moreover, UV radiation from sunlight can regulate numerous ferroptosis-linked genes. This review will focus on the function of ferroptosis in UV radiation-damaged skin cells. We hope to draw attention to the significance of ferroptosis regulation in the prevention and treatment of skin photoaging.