Graves’ ophthalmopathy (GO), also known as thyroid-associated orbitopathy, is a disfiguring and potentially sight-threatening ocular disease. GO is an autoimmune inflammatory disorder, characterized by increased fibroadipose tissue and extraocular muscle volume within the limited orbital space. Although a clear and indisputable mechanism of the pathogenesis of GO remains to be established, the disease often presents initially as an inflammatory response and is followed by a tissue remodelling and/or fibrogenic process.

Current treatments using corticosteroid and radiotherapy are sometimes effective in alleviating the inflammatory symptoms of the disease, but there remains a challenge for physicians to prevent or reverse pathological changes of orbital tissues. Elucidation of the molecular mechanisms of GO is crucial for the development of novel treatments.

This Special Issue aims to collect papers that can be integrated into a common purpose: that of furthering the understanding of the molecular mechanisms that initiate and regulate the process of inflammation and tissue remodeling in GO. Novel management and review articles are also welcomed.

Potential topics include but are not limited to the following:

• Novel molecular mechanisms for GO
• Molecular targets in GO for monoclonal antibody therapy approaches
• New potential biomarkers involved in GO
• Oxidative stress in GO
• Biological and clinical effects of smoking on GO
• The emerging role of epigenetics in patients with GO
• New trends in the management of patients with GO