Reactive oxygen species (ROS), such as superoxides (O₂•−) and hydroxyl groups (OH·), are short-lived molecules containing unpaired electrons. Intracellular ROS are primarily produced by mitochondria and NADPH oxidase (NOX) and are involved in various physiological processes, including proliferation, cell signaling, and oxygen homeostasis. Recent studies have highlighted the crucial role of ROS in regulating ultraviolet (UV)-induced photodamage of the skin, which accounts for 80% of skin aging. This review elaborates on the biological characteristics of ROS and its role in UV-induced photodamage. UV radiation, composed of UVC, UVB, and UVA, can penetrate the ozone layer and cause dermal photodamage through DNA damage, inflammation, oxidative stress, and apoptosis. ROS play a central role in these processes by regulating DNA damage, cell signaling pathways, and collagen metabolism. They can induce DNA damage, leading to cell death and the release of inflammatory cytokines. Additionally, ROS are involved in UV-induced mitochondrial apoptosis by affecting the expression of Bcl-2 and Bcl-x, leading to the release of cytochrome c and subsequent apoptosis. The review also discusses the signaling pathways of ROS in UV-induced photodamage, including the MAPK, NF-κB, and AP-1 pathways. These pathways regulate the expression of inflammatory factors and matrix metalloproteinases (MMPs), leading to collagen degradation and skin relaxation. Furthermore, ROS can disrupt the balance between pro- and anti-apoptotic proteins, accelerating cell death and contributing to skin cancer. In conclusion, ROS play a central role in UV-induced photodamage, and understanding their detailed signaling pathways is crucial for developing effective treatments and preventing skin damage.Reactive oxygen species (ROS), such as superoxides (O₂•−) and hydroxyl groups (OH·), are short-lived molecules containing unpaired electrons. Intracellular ROS are primarily produced by mitochondria and NADPH oxidase (NOX) and are involved in various physiological processes, including proliferation, cell signaling, and oxygen homeostasis. Recent studies have highlighted the crucial role of ROS in regulating ultraviolet (UV)-induced photodamage of the skin, which accounts for 80% of skin aging. This review elaborates on the biological characteristics of ROS and its role in UV-induced photodamage. UV radiation, composed of UVC, UVB, and UVA, can penetrate the ozone layer and cause dermal photodamage through DNA damage, inflammation, oxidative stress, and apoptosis. ROS play a central role in these processes by regulating DNA damage, cell signaling pathways, and collagen metabolism. They can induce DNA damage, leading to cell death and the release of inflammatory cytokines. Additionally, ROS are involved in UV-induced mitochondrial apoptosis by affecting the expression of Bcl-2 and Bcl-x, leading to the release of cytochrome c and subsequent apoptosis. The review also discusses the signaling pathways of ROS in UV-induced photodamage, including the MAPK, NF-κB, and AP-1 pathways. These pathways regulate the expression of inflammatory factors and matrix metalloproteinases (MMPs), leading to collagen degradation and skin relaxation. Furthermore, ROS can disrupt the balance between pro- and anti-apoptotic proteins, accelerating cell death and contributing to skin cancer. In conclusion, ROS play a central role in UV-induced photodamage, and understanding their detailed signaling pathways is crucial for developing effective treatments and preventing skin damage.