| Summary: | Thyroid Eye Disease (TED) is a debilitating autoimmune condition characterized by significant inflammation of orbital tissues, including the extraocular muscles and adipose tissues. The pathological mechanisms underlying this inflammation involve a complex interplay of stress responses at the cellular and molecular level. This review aims to critically evaluate and synthesize existing literature on the mechanisms of orbital inflammation in TED. We discuss the role of autoantibodies, cytokines, and reactive oxygen species (ROS) in the initiation and propagation of the inflammatory process. Additionally, we explore how stress responses triggered by these elements affect the integrity of orbital tissues and contribute to its remodeling. Our review underscores the need for continued research in this field, which may pave the way for novel therapeutic strategies for TED.
|
|---|