ReviewFrontiers in cell and developmental biology2024
The role of autophagy in Graves disease: knowns and unknowns.
Review in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Placental dysfunction, inflammation, and impaired autophagy in preeclampsia: A pathophysiological link to autism spectrum disorder.Metabolic brain disease · 2026Review
- Peripheral blood inflammatory indices across thyroid functional states in Graves' disease: associations with liver biochemical abnormalities and hyperthyroid relapse.Frontiers in endocrinology · 2026Article
- Interconnection between myasthenia gravis and type 2 diabetes: emerging role of metformin in modulating PI3K/AKT/mTOR/AMPK axis.Metabolic brain disease · 2025Review
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10 authors.
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Abstract
Graves disease (GD), an autoimmune disease affects the thyroid gland, results in hyperthyroidisms and goiter. The main cause of GD is not clearly defined; however, stimulating autoantibodies for thyroid stimulating hormone receptor (TSHR) known as thyroid-stimulating immunoglobulins (TSIs) are the primary proposed mechanism. The TSI activation of TSHRs of thyroid gland results in excessive release of thyroid hormones with the subsequent development of hyperthyroidism and goiter. The cellular process of macroautophagy/autophagy is implicated in the pathogenesis of GD and other thyroid diseases. Autophagy plays a critical role in many thyroid diseases and in different stages of the same disease through modulation of immunity and the inflammatory response. In addition, autophagy is also implicated in the pathogenesis of thyroid-associated ophthalmopathy (TAO). However, the exact role of autophagy in GD is not well explained. Therefore, this review discusses how autophagy is intricately involved in the pathogenesis of GD regarding its protective and harmful effects.
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