Thyroid-associated ophthalmopathy(TAO)is the most common orbital disease and is a specific autoimmune disorder, of which the etiology and pathogenesis is still unclear. TAO can affect the appearance and visual function of patients, and severe cases can lead to blindness. Tissue currently considered excessive expansion due to orbital fat is formed of one of the key pathological features TAO. The increase of orbital adipose tissue can directly lead to increased retrobulbar pressures and eyeball protrusion. As a new endocrine organ, adipose tissue can secrete a variety of adipocytokines, growth factors and protein molecules, some of which may be involved in the pathogenesis of TAO. The role of abnormal adipose tissue proliferation of TAO is reviewed from the expression of key proteins of adipose differentiation, autophagy, retrobulbar pressure and hypoxia.