Evidence map›Paper›PMID 28127991›Full record

ReviewExpert opinion on therapeutic targets2017

TSHR as a therapeutic target in Graves' disease.

Terry Smith

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Novel Antimurine Thyroid-Stimulating Hormone Receptor Monoclonal Antibodies.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2023
    Article
  4. Comparison Between Thyroid Stimulating Immunoglobulin and TSH-Receptor Antibodies in the Management of Graves' Orbitopathy.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2023
    Article
  5. Review
  6. Review
  7. Serum thyroglobulin is associated with orbitopathy in Graves' disease.Journal of endocrinological investigation · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Immunological Aspects of Graves' Ophthalmopathy.BioMed research international · 2019
    Review
  14. Graves Disease in Central Ghana: Clinical Characteristics and Associated Factors.Clinical medicine insights. Endocrinology and diabetes · 2018
    Article
  15. Review
  16. Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Terry Smitha Department of Ophthalmology and Visual Sciences , University of Michigan , Ann Arbor , MI , USA.
University of Michigan–Ann Arbor · US

Funding

REGULATION OF RETROOCULAR CONNECTIVE TISSUER01EY008976 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SMITH, TERRY J · 1993 to 2020
$6.4M
University of Michigan Autoimmunity Center of Excellence, Clinical Research ProgrUM1AI110557 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 2014 to 2018
$543k
CHLAMYDIA GENETICS AND OCULAR DISEASEF32EY007002 · NEI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI KANE, COLLEEN D · 1999 to 2002
$79k
NEI NIH HHS F32 EY007002NEI NIH HHS R01 EY008976NIAID NIH HHS UM1 AI110557
6 · The paper itself

Abstract

introductionGraves' disease (GD) and thyroid-associated ophthalmopathy (TAO) are thought to result from actions of pathogenic antibodies mediated through the thyrotropin receptor (TSHR). This leads to the unregulated consequences of the antibody-mediated receptor activity in the thyroid and connective tissues of the orbit. Recent studies reveal antibodies that appear to be directed against the insulin-like growth factor-I receptor (IGF-IR). Areas covered: In this brief article, I attempt to review the fundamental characteristics of the TSHR, its role in GD and TAO, and its relationship to IGF-IR. Strong evidence supports the concept that the two receptors form a physical and functional complex and that IGF-IR activity is required for some of the down-stream signaling initiated through TSHR. Recently developed small molecules and monoclonal antibodies that block TSHR and IGF-IR signaling are also reviewed in the narrow context of their potential utility as therapeutics in GD and TAO. The Pubmed database was searched from its inception for relevant publications. Expert opinion: Those agents that can interrupt the TSHR and IGF-IR pathways possess the potential for offering more specific and better tolerated treatments of both hyperthyroidism and TAO. This would spare patients exposure to toxic drugs, ionizing radiation and potentially hazardous surgeries.

Indexed as

AnimalsAntibodiesAntibodies, MonoclonalDrug DesignGraves DiseaseGraves OphthalmopathyHumansMolecular Targeted TherapyReceptor, IGF Type 1Receptors, ThyrotropinAntibodiesAntibodies, MonoclonalReceptor, IGF Type 1Receptors, ThyrotropinAutoimmunityGraves’ diseaseophthalmopathytyrosine kinase

Identifiers

PMID28127991
PMCPMC5718165
OpenAlexW2580160816

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.