biostudies-literatureUnknown29(1)Kim YGOral lichen planus (OLP) is a chronic inflammatory condition characterized by CD8+ T cell-mediated apoptosis of oral epithelial cells. While psychological stress has been implicated in OLP pathogenesis, the underlying mechanisms remain unclear. This study explores the role of epinephrine, a primary stress-related catecholamine, in OLP progression. We found that high concentrations of epinephrine induce cytotoxicity in oral keratinocytes, marked by reduced cell viability and increased DNA damage. High-dose epinephrine also elevates oxidative stress by downregulating antioxidant proteins SOD2 and SESN2. Additionally, it activates the STAT3 signaling pathway through both alpha- and beta-adrenergic receptors. Furthermore, epinephrine increases levels of HMGB1 and extracellular ATP, key damage-Animal cells and systems653-664https://www.ebi.ac.uk/biostudies/studies/S-EPMC12624973biostudies-literatureEpinephrine as a potential driver of oral lichen planus pathogenesis.PMC12624973Song HJJung WByun JSJang SKim DYKang KHKim YGfalseEpinephrine as a potential driver of oral lichen planus pathogenesis.Oral lichen planus (OLP) is a chronic inflammatory condition characterized by CD8+ T cell-mediated apoptosis of oral epithelial cells. While psychological stress has been implicated in OLP pathogenesis, the underlying mechanisms remain unclear. This study explores the role of epinephrine, a primary stress-related catecholamine, in OLP progression. We found that high concentrations of epinephrine induce cytotoxicity in oral keratinocytes, marked by reduced cell viability and increased DNA damage. High-dose epinephrine also elevates oxidative stress by downregulating antioxidant proteins SOD2 and SESN2. Additionally, it activates the STAT3 signaling pathway through both alpha- and beta-adrenergic receptors. Furthermore, epinephrine increases levels of HMGB1 and extracellular ATP, key damage-2025-01-01T00:00:00Z20252026-06-05T19:21:31.186Z2026-05-20T03:14:09.595ZS-EPMC126249734126232410.1080/19768354.2025.2588914