Evidence map›Paper›PMID 34496027›Full record

ArticleEndocrinology2021

Simulation Model for Hashimoto Autoimmune Thyroiditis Disease.

Marcela Salazar-Viedma, Juan Gabriel Vergaño-Salazar, Luis Pastenes, Vivian D'Afonseca

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Nutritional Management of Thyroiditis of Hashimoto.International journal of molecular sciences · 2022
    Review
  11. Psoriasis and Systemic Inflammatory Disorders.International journal of molecular sciences · 2022
    Review
  12. 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

4 authors at 1 institution in 1 country.

Marcela Salazar-ViedmaLaboratorio de Genética y Microevolución, Facultad de Ciencias Básicas, Universidad Católica del Maule, Talca 3466706, Chile.ORCID 0000-0001-7065-8842
Juan Gabriel Vergaño-SalazarDoctorado en Modelamiento Matemático Aplicado, Facultad de Ciencias Básicas, Universidad Católica del Maule, Talca 3466706, Chile.ORCID 0000-0003-2626-7558
Luis PastenesLaboratorio de Genética y Microevolución, Facultad de Ciencias Básicas, Universidad Católica del Maule, Talca 3466706, Chile.
Vivian D'AfonsecaCentro de Investigación y Estudios Avanzados del Maule (CIEAM), Vicerrectoría de Investigación y Posgrado, Universidad Católica del Maule, Talca 3466706, Chile.
Catholic University of the Maule · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hashimoto thyroiditis (HT) is a pathology that often causes a gradual thyroid insufficiency in affected patients due to the autoimmune destruction of this gland. The cellular immune response mediated by T helper lymphocytes TH1 and TH17 can induce the HT disease. In this pathologic condition, there is an imbalance between the TH17 and Treg lymphocytes as well as a gut microbiota dysfunction. The objective of this work was to describe the interactions of the cell subpopulations that participate in HT. To achieve this goal, we generated a mathematical model that allowed the simulation of different scenarios for the dynamic interaction between thyroid cells, the immune system, and the gut microbiota. We used a hypothetical-deductive design of mathematical modeling based on a system of ordinary differential equations, where the state variables are the TH1, TH17, and Treg lymphocytes, the thyrocytes, and the bacteria from gut microbiota. This work generated a compartmental model of the cellular immune response occurring in the thyroid gland. It was observed that TH1 and TH17 lymphocytes could increase the immune cells' activity, as well as activate effector cells directly and trigger the apoptosis and inflammation processes of healthy thyrocytes indirectly. Likewise, the model showed that a reduction in Treg lymphocytes could increase the activity of TH17 lymphocytes when an imbalance of the gut microbiota composition occurred. The numerical results highlight the TH1, TH17, and bacterial balance of the gut microbiota activities as important factors for the development of HT disease.

Indexed as

Models, TheoreticalAnimalsComputer SimulationGastrointestinal MicrobiomeHashimoto DiseaseHumansTh17 CellsThyroid Epithelial CellsThyroiditis, AutoimmuneT-Lymphocytes, Regulatoryautoimmune hypothyroidismdynamic systemsgut microbiotamathematical modelingT helper cellsthyrocytes

Identifiers

PMID34496027
PMCPMC8477452
OpenAlexW3196355178

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.