Evidence map›Paper›PMID 34501407›Full record

ArticleJournal of clinical medicine2021

+3179G/A Insulin-Like Growth Factor-1 Receptor Polymorphism: A Novel Susceptibility Contributor in Anti-Ro/SSA Positive Patients with Sjögren's Syndrome: Potential Clinical and Pathogenetic Implications.

Charalampos Skarlis, Nikolaos Marketos, Adrianos Nezos, Asimina Papanikolaou, Michael Voulgarelis, Michael Koutsilieris, Haralampos M Moutsopoulos, Clio P Mavragani

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Article
  4. Sjogren's Syndrome: Recent Updates.Journal of clinical medicine · 2022
    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

8 authors at 2 institutions in 1 country.

Charalampos SkarlisDepartment of Physiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0002-1781-2799
Nikolaos MarketosDepartment of Physiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.ORCID 0000-0001-6995-3713
Adrianos NezosDepartment of Physiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Asimina PapanikolaouDepartment of Hematopathology, Evangelismos Hospital, 11527 Athens, Greece.
Michael VoulgarelisDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Michael KoutsilierisDepartment of Physiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Haralampos M MoutsopoulosDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Clio P MavraganiDepartment of Physiology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.
National and Kapodistrian University of Athens · GREvangelismos Hospital · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlterations of the insulin-like growth factor (IGF) pathway along with genetic variations of the IGF1 receptor (IGF1R) gene have been linked to the development of systemic autoimmunity, possibly through apoptosis induction. This study aims to investigate whether genetic variations of the IGF1R contribute to Sjögren's syndrome (SS) pathogenesis and explores potential functional implications.

methodsDNA extracted from whole peripheral blood derived from 277 primary SS patients, complicated or not by lymphoma, and 337 Healthy controls (HC) was genotyped for the rs2229765 IGF1R polymorphism using the RFLP-PCR assay. Gene expression of IGF1R and IGF1 isoforms, caspases 1, 4, and 5, and inflammasome components NLRP3, ASC, IL1β, IL18, IL33, IGFBP3, and IGFBP6 were quantitated by RT-PCR in total RNA extracted from minor salivary gland biopsies (MSGs) of 50 SS patients and 13 sicca controls (SCs). In addition, IGF1R immunohistochemical (IHC) expression was assessed in formalin-fixed, paraffin-embedded MSG tissue sections derived from 10 SS patients and 5 SCs.

resultsThe prevalence of the A/A genotype of the rs2229765 IGF1R polymorphism was significantly higher in the anti-Ro/SSA positive SS population compared to healthy controls (24.8% vs. 10.7%,

conclusionsThe rs2229765 IGF1R variant confers increased susceptibility for seropositive primary SS. Dampened IGF1R mRNA and protein expression in salivary gland tissues could be related to increased apoptosis and subsequently to the activation of inflammasome pathways.

Indexed as

anti-Ro/SSAautoimmunityinsulin growth factor receptorpyroptosisrs2229765Sjögren’s syndrome

Identifiers

PMID34501407
PMCPMC8432056
OpenAlexW3198866935

What Socratic holds

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LicenceCC BY
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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 Socratic graph.