Oxidative stress pathways in skin

Oxidative stress pathways in the skin represent a complex network of biochemical processes triggered by an imbalance between the production of reactive oxygen species (ROS) and the skin's antioxidant defense mechanisms [1, 2]. These pathways are primarily activated by external stressors such as ultraviolet (UV) radiation, environmental pollution, and chemical exposure, as well as internal metabolic byproducts [3, 4]. Key molecular components involved include the Nrf2 transcription factor, which orchestrates the antioxidant response, and pro-inflammatory signaling mediators like NF-kB and the MAPK family [1, 5]. Chronic or excessive activation of these pathways leads to significant cellular damage, including lipid peroxidation, protein carbonylation, and DNA mutations [2, 4]. Such damage is a fundamental driver of skin aging (photoaging), chronic inflammatory conditions like dermatitis, and the initiation of skin carcinogenesis [1, 4, 5]. Therapeutic interventions typically focus on restoring redox balance through the application of exogenous antioxidants like vitamins C and E or by modulating endogenous pathways using Nrf2 activators [10, 11]. Additionally, inhibiting downstream effectors like matrix metalloproteinases (MMPs) helps preserve the structural integrity of the dermal extracellular matrix [1, 4]. Understanding these integrated pathways is essential for the development of effective dermocosmetic and pharmacological treatments aimed at protecting the skin from environmental damage [11].

Other names

Cutaneous oxidative stress signalingSkin antioxidant defense systemReactive oxygen species (ROS) pathways in skinRedox signaling in skin

Neutralization of reactive oxygen species (ROS), activation of the Nrf2-mediated antioxidant response element (ARE) pathway, inhibition of pro-inflammatory NF-kB and MAPK signaling, and upregulation of endogenous antioxidant enzymes such as superoxide dismutase and catalase [1, 5, 11].