Abstract
Graves’ ophthalmopathy (GO) is the most common extrathyroidal manifestation of Graves’ disease. It is characterized initially by an inflammatory process, followed by tissue remodeling and fibrosis, leading to proptosis, exposure keratopathy, ocular motility limitation, and compressive optic neuropathy. The pathogenic mechanism is complex and multifactorial. Accumulating evidence suggests the involvement of oxidative stress in the pathogenesis of GO. Cigarette smoking, a major risk factor for GO, has been shown to induce reactive oxygen species (ROS) generation and oxidative damage in GO orbital fibroblasts. In addition, an elevation in ROS and antioxidant enzymes is observed in tears, blood, and urine, as well as orbital fibroadipose tissues and fibroblasts from GO patients. In vitro and in vivo studies have examined the efficacy of various antioxidant supplements for GO. These findings suggest a therapeutic role of antioxidants in GO patients. This review summarizes the current understanding of oxidative stress in the pathogenesis and potential antioxidants for the treatment of GO.
Highlights
Graves’ ophthalmopathy (GO) is known as thyroid-associated ophthalmopathy (TAO) and thyroid eye disease (TED)
One recent study further demonstrated that the production of hyaluronan and inflammatory cytokines (IL-1α, IL-8, and TNFα), as well as the generation of intracellular reactive oxygen species (ROS) were suppressed by selenium in cultured GO orbital fibroblasts [71]
This review summarizes the current understanding of oxidative stress in the pathogenesis of GO and potential antioxidants for the treatment of GO
Summary
Graves’ ophthalmopathy (GO) is known as thyroid-associated ophthalmopathy (TAO) and thyroid eye disease (TED). Orbital fibroblasts interact with circulating T cells and respond to autoantibodies produced by B cells as well as various cytokines and perhaps as yet unrecognized stimuli. They proliferate and secrete glycosaminoglycans (GAGs), in particular hyaluronan, into the extracellular matrix (ECM), and differentiate into adipocytes or myofibroblasts. We summarize the current clinical and experimental findings regarding oxidative stress in the disease process as well as the potential role of antioxidants in GO. This supports the advance in antioxidants for the treatment of GO
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