ReviewBest practice & research. Clinical endocrinology & metabolism2012
Role of insulin-like growth factor-1 (IGF-1) pathway in the pathogenesis of Graves' orbitopathy.
Review in Best practice & research. Clinical endocrinology & metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 135 citations in OpenAlex.
- Serum free fatty acid profiles as novel biomarkers for disease activity in Graves' orbitopathy.Journal of endocrinological investigation · 2026Article
- Epigenetic Modulation of Thyroid-Stimulating Hormone Receptor Expression in Orbital Fibroblasts From Graves' Ophthalmopathy: Target for Treatment.Investigative ophthalmology & visual science · 2026Article
- Metformin inhibits PDGFβ signaling to suppress hyaluronan and cytokine production in thyroid eye disease.Experimental eye research · 2026Article
- Pegvisomant in severe, treatment-resistant thyroid eye disease: a case report.Drugs in context · 2026Article
- The therapeutic revolution in thyroid eye disease: from orbital radiotherapy to teprotumumab and AI.Frontiers in medicine · 2026Review
- Article
- Three-Dimensional Culture of Orbital Fibroblasts From Thyroid Eye Disease Induce In Vivo-Like Tissue Remodeling and Fibrosis.Investigative ophthalmology & visual science · 2025Article
- Canonical and Truncated Transglutaminase-2 Drive TGF-β1 Autocrine Loop to Induce Fibrosis in Graves' Orbitopathy.Investigative ophthalmology & visual science · 2025Article
- Targeting the Aryl Hydrocarbon Receptor to Attenuate IGF1R Signaling in Thyroid Eye Disease.Thyroid : official journal of the American Thyroid Association · 2025Article
- Effects of linsitinib on M22 and IGF:1-treated 3D spheroids of human orbital fibroblasts.Scientific reports · 2025Article
- Glymphatic System Dysfunction in Thyroid Eye Disease Associated with Disease Activity and Duration.Journal of inflammation research · 2025Article
- Endoplasmic reticulum protein TXNDC5 modulates thyroid eye disease TGF-β1-induced myofibroblast transdifferentiation.BMJ open ophthalmology · 2024Article
- Transcriptomic profiling of thyroid eye disease orbital fat demonstrates differences in adipogenicity and IGF-1R pathway.JCI insight · 2024Article
- Role of Lysyl Oxidase-Like Protein 3 in the Pathogenesis of Graves' Orbitopathy in Orbital Fibroblasts.Investigative ophthalmology & visual science · 2024Article
- A Biologic and Physical Characterization of an Injectable Amniotic Membrane Designed for Treating Diabetic Foot Ulcers.Bioengineering (Basel, Switzerland) · 2024Article
- The Role of Fibrogenesis and Extracellular Matrix Proteins in the Pathogenesis of Graves' Ophthalmopathy.International journal of molecular sciences · 2024Review
- SOX9 Induces Orbital Fibroblast Activation in Thyroid Eye Disease Via MAPK/ERK1/2 Pathway.Investigative ophthalmology & visual science · 2024Article
- Thyroid-associated ophthalmopathy and ferroptosis: a review of pathological mechanisms and therapeutic strategies.Frontiers in immunology · 2024Review
- Article
- Unexpected Crosslinking Effects of a Human Thyroid Stimulating Monoclonal Autoantibody, M22, with IGF1 on Adipogenesis in 3T3L-1 Cells.International journal of molecular sciences · 2023Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The etiology of Graves' orbitopathy (GO) remains enigmatic and thus controversy surrounds its pathogenesis. The role of the thyroid stimulating hormone receptor (TSHR) and activating antibodies directed against it in the hyperthyroidism of Graves' disease (GD) is firmly established. Less well elucidated is what part the TSHR pathway might play in the development of GO. Also uncertain is the participation of other cell surface receptors in the disease. Elevated levels of insulin-like growth factor-1 receptor (IGF-1R) have been found in orbital fibroblasts as well as B and T cells from patients with GD. These abnormal patterns of IGF-1R display are also found in rheumatoid arthritis and carry functional consequences. In addition, activating IgGs capable of displacing IGF-1 from IGF-1R have also been detected in patients with these diseases. IGF-1R forms a complex with TSHR which is necessary for at least some of the non-canonical signaling observed following TSHR activation. Functional TSHR and IGF-1R have also been found on fibrocytes, CD34⁺ bone marrow-derived cells from the monocyte lineage. Levels of TSHR on fibrocytes greatly exceed those found on orbital fibroblasts. When ligated by TSH or M22, a TSHR-activating monoclonal antibody, fibrocytes produce extremely high levels of several cytokines and chemokines. Moreover, fibrocytes infiltrate both the orbit and thyroid in GD. In sum, based on current evidence, IGF-1R and TSHR can be thought of as "partners in crime". Involvement of the former probably transcends disease boundaries, while TSHR may not.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.