Evidence map›Paper›PMID 22116709›Full record

ReviewClinical reviews in allergy & immunology2012

Autoimmune diseases and polyamines.

Wesley H Brooks

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05594563 (TArgeting Type 1 Diabetes Using POLyamines), which is not on this map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 18% 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.

NCT05594563 phase2active not recruitingnot on this mapstarted 2023, after this paper: background citation

TArgeting Type 1 Diabetes Using POLyamines (TADPOL): A Randomized, Double-Masked, Placebo-Controlled Phase 2 Study to Evaluate the Efficacy and Safety of Difluoromethylornithine (DFMO) to Preserve Insulin Production in Type 1 Diabetes

TypeinterventionalSponsorEmily K. SimsRan2023 to 2027Enrolled74ConditionsType 1 DiabetesArmsDFMO, Placebo
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Sex-related differences in urinary immune-related metabolic profiling of alopecia areata patients.Metabolomics : Official journal of the Metabolomic Society · 2020
    Article
  10. Review
  11. Review
  12. Epigenetics in the pathogenesis of RA.Seminars in immunopathology · 2017
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Molecular mechanisms in autoimmune type 1 diabetes: a critical review.Clinical reviews in allergy & immunology · 2014
    Review
  18. Article
  19. Review
  20. 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.

Wesley H BrooksExperimental HTS, SRB-3, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612-9416, USA. wesley.brooks@moffitt.org
Moffitt Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetics and environmental factors have important roles in autoimmune diseases but neither has given us sufficient understanding of these mysterious diseases. Therefore, we are now looking closer at epigenetics, an interface between genetics and environmental factors. Epigenetics can be defined as reversible heritable changes to chromatin that can alter gene expression without altering the gene's DNA sequence. Methylation of DNA and histones are primary means of epigenetic control. By adding methyl groups to DNA and histones, it can limit accessibility of the underlying gene thereby altering the amount of gene expression. The methyl group is derived from an essential molecule in the cell, S-adenosylmethionine (SAM). However, a group of small molecules called polyamines also require SAM for their synthesis. Polyamines are essential for many cellular functions and polyamine activity is increased in many autoimmune diseases. Presented here is the "polyamine hypothesis" in which increased polyamine synthesis competes with cellular methylation (epigenetic control) for SAM. It is proposed that increased polyamine activity can cause disruption of cellular methylation, which can lead to abnormal expression of previously sequestered genes and disruption of other methylation-dependent cellular processes.

Indexed as

AnimalsAutoimmune DiseasesEpigenomicsHumansMethylationPolyaminesS-AdenosylmethioninePolyaminesS-Adenosylmethionine

Identifiers

PMID22116709
OpenAlexW2002077458

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.