Autoimmune uveitis (AU) and mood disorders, such as anxiety and depression, share a close bidirectional association. Visual impairment caused by AU and the side effects of glucocorticoid therapy significantly increase the incidence of anxiety and depression. Conversely, mood disorders disrupt immune homeostasis through neuro-endocrine-immune mechanisms, exacerbating inflammatory responses and elevating the risk of AU recurrence. The primary reasons for AU-induced mood disorders include visual impairment, unpredictable fluctuations in vision, long-term treatment, and glucocorticoid-related psychiatric reactions. Meanwhile, mood disorders not only trigger the onset and recurrence of AU but also interfere with treatment efficacy by reducing patient adherence. The underlying mechanisms involve psychological stress leading to hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, inflammatory factor-mediated “brain-eye axis” regulation, synergistic effects of the gut microbiota-brain-immune axis, and stage-specific immune regulatory characteristics of acute and chronic stress. Therefore, clinical management should emphasize the synergistic integration of psychological interventions and anti-inflammatory therapy to enable early detection and treatment of extramedullary lesions, optimize diagnostic and therapeutic protocols, and improve the prognosis of AU patients. Future research should further elucidate the molecular mechanisms underlying the interaction between mood and inflammation, establish multidisciplinary collaborative diagnosis and treatment systems, validate the efficacy of psychological interventions through large-scale clinical studies, and explore the development of neuroprotective anti-inflammatory drugs.
Iron death is an alternative to normal cell death and is regulated by a variety of cellular metabolic pathways. Iron death has become a hot topic of research because it can cause damage to various organs and degenerative diseases in the body. Metabolism, signalling pathways, endoplasmic reticulum stress, and immune cells can all affect the occurrence of iron death, and the blood-retina destruction induced by iron death plays an important role in autoimmune uveitis. Exploring the components of the blood-retina regulatory mechanism of iron death in autoimmune uveitis can lead to the search for targeted drug targets, which can provide a new research idea for the subsequent study of the diagnosis and treatment of autoimmune uveitis.