The miR-320a/PRDX3 Axis Alleviates the Oxidative Stress and Fibrotic Alterations in Fibroblasts in Thyroid Eye Disease

The study highlights the critical role of miR-320a in TED pathogenesis through its regulation of orbital fibroblast (OF) activation, fibrosis, oxidative stress, and the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway, mediated by its interaction with PRDX3. Targeting the miR-320a/PRDX3 axis represents a promising therapeutic strategy to alleviate the oxidative stress and fibrotic alterations in TED, underscoring the potential of miR-320a as a therapeutic target in managing TED progression.