The role of autophagy in Graves disease: knowns and unknowns
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 p...
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Frontiers Media S.A.
2025-01-01
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| Series: | Frontiers in Cell and Developmental Biology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2024.1480950/full |
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| author | Hayder M. Al-kuraishy Ghassan M. Sulaiman Hamdoon A. Mohammed Mohammed H. Abu-Alghayth Salim Albukhaty Majid S. Jabir Ali K. Albuhadily Ali I. Al-Gareeb Daniel J. Klionsky Mosleh M. Abomughaid |
| author_facet | Hayder M. Al-kuraishy Ghassan M. Sulaiman Hamdoon A. Mohammed Mohammed H. Abu-Alghayth Salim Albukhaty Majid S. Jabir Ali K. Albuhadily Ali I. Al-Gareeb Daniel J. Klionsky Mosleh M. Abomughaid |
| author_sort | Hayder M. Al-kuraishy |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-15901e444bc84b14947dc8138c649d7c |
| institution | Kabale University |
| issn | 2296-634X |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cell and Developmental Biology |
| spelling | doaj-art-15901e444bc84b14947dc8138c649d7c2025-01-06T06:59:39ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2025-01-011210.3389/fcell.2024.14809501480950The role of autophagy in Graves disease: knowns and unknownsHayder M. Al-kuraishy0Ghassan M. Sulaiman1Hamdoon A. Mohammed2Mohammed H. Abu-Alghayth3Salim Albukhaty4Majid S. Jabir5Ali K. Albuhadily6Ali I. Al-Gareeb7Daniel J. Klionsky8Mosleh M. Abomughaid9Department of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, IraqDivision of Biotechnology, Department of Applied Sciences, University of Technology, Baghdad, IraqDepartment of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, Qassim University, Qassim, Saudi ArabiaDepartment of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Bisha, Bisha, Saudi ArabiaDepartment of Laboratory Techniques, Al-Manara College for Medical Sciences, Maysan, IraqDivision of Biotechnology, Department of Applied Sciences, University of Technology, Baghdad, IraqDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, IraqDepartment of Clinical Pharmacology and Medicine, Jabir Ibn Hayyan Medical University, Najaf, IraqLife Sciences Institute, University of Michigan, Ann Arbor, MI, United StatesDepartment of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Bisha, Bisha, Saudi ArabiaGraves 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.https://www.frontiersin.org/articles/10.3389/fcell.2024.1480950/fullautoantibodiesautophagyGraves diseasepathogenesisthyroid-associated ophthalmopathy |
| spellingShingle | Hayder M. Al-kuraishy Ghassan M. Sulaiman Hamdoon A. Mohammed Mohammed H. Abu-Alghayth Salim Albukhaty Majid S. Jabir Ali K. Albuhadily Ali I. Al-Gareeb Daniel J. Klionsky Mosleh M. Abomughaid The role of autophagy in Graves disease: knowns and unknowns Frontiers in Cell and Developmental Biology autoantibodies autophagy Graves disease pathogenesis thyroid-associated ophthalmopathy |
| title | The role of autophagy in Graves disease: knowns and unknowns |
| title_full | The role of autophagy in Graves disease: knowns and unknowns |
| title_fullStr | The role of autophagy in Graves disease: knowns and unknowns |
| title_full_unstemmed | The role of autophagy in Graves disease: knowns and unknowns |
| title_short | The role of autophagy in Graves disease: knowns and unknowns |
| title_sort | role of autophagy in graves disease knowns and unknowns |
| topic | autoantibodies autophagy Graves disease pathogenesis thyroid-associated ophthalmopathy |
| url | https://www.frontiersin.org/articles/10.3389/fcell.2024.1480950/full |
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