Evidence map›Paper›PMID 34573074›Full record

ArticleAntioxidants (Basel, Switzerland)2021

The Influence of Oxidative Stress on Thyroid Diseases.

Joanna Kochman, Karolina Jakubczyk, Piotr Bargiel, Katarzyna Janda-Milczarek

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
15.4field-weighted citation impact, top 1% 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

84 citing papers in PubMed, 171 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Food science & nutrition · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Thyroid Hormone T3 Induces DNA Damage Response in Breast Cancer Cells.International journal of molecular sciences · 2026
    Article
  12. Single-Cell RNA Sequencing of Thyroid Tissues Reveals Pathogenesis of Graves' Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

24 more citing papers are in PubMed but not listed here.

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.

Joanna KochmanDepartment of Human Nutrition and Metabolomics, Pomeranian Medical University, 24 Broniewskiego Street, 71-460 Szczecin, Poland.ORCID 0000-0002-7863-3241
Karolina JakubczykDepartment of Human Nutrition and Metabolomics, Pomeranian Medical University, 24 Broniewskiego Street, 71-460 Szczecin, Poland.ORCID 0000-0002-5853-9709
Piotr BargielClinic of Plastic, Endocrine and General Surgery, Pomeranian Medical University, 2 Siedlecka Street, 72-010 Police, Poland.
Katarzyna Janda-MilczarekDepartment of Human Nutrition and Metabolomics, Pomeranian Medical University, 24 Broniewskiego Street, 71-460 Szczecin, Poland.ORCID 0000-0002-4548-3419
Pomeranian Medical University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroid diseases, including neoplasms, autoimmune diseases and thyroid dysfunctions, are becoming a serious social problem with rapidly increasing prevalence. The latter is increasingly linked to oxidative stress. There are many methods for determining the biomarkers of oxidative stress, making it possible to evaluate the oxidative profile in patients with thyroid diseases compared to the healthy population. This opens up a new perspective for investigating the role of elevated parameters of oxidative stress and damage in people with thyroid diseases, especially of neoplastic nature. An imbalance between oxidants and antioxidants is observed at different stages and in different types of thyroid diseases. The organ, which is part of the endocrine system, uses free radicals (reactive oxygen species, ROS) to produce hormones. Thyroid cells release enzymes that catalyse ROS generation; therefore, a key role is played by the internal defence system and non-enzymatic antioxidants that counteract excess ROS not utilised to produce thyroid hormones, acting as a buffer to neutralise free radicals and ensure whole-body homeostasis. An excess of free radicals causes structural cell damage, undermining genomic stability. Looking at the negative effects of ROS accumulation, oxidative stress appears to be implicated in both the initiation and progression of carcinogenesis. The aim of this review is to investigate the oxidation background of thyroid diseases and to summarise the links between redox imbalance and thyroid dysfunction and disease.

Indexed as

antioxidantsoxidative stressROSthyroid diseases

Identifiers

PMID34573074
PMCPMC8465820
OpenAlexW3200513687

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.