Evidence map›Paper›PMID 32613397›Full record

ReviewClinical rheumatology2021

The multifaceted functional role of DNA methylation in immune-mediated rheumatic diseases.

Matteo Vecellio, Haijing Wu, Qianjin Lu, Carlo Selmi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical rheumatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Epigenetic regulation of 15-lipoxygenase-1 expression in human chondrocytes by promoter methylation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  8. Review
  9. DNA Methylation Expression Profile of Blood Heat Syndrome and Blood Stasis Syndrome in TCM Psoriasis.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Ten Years of EWAS.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Review
  14. Article
  15. 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 2 institutions in 3 countries.

Matteo Vecellio *Division of Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center, IRCCS, via Manzoni 56, 20089 Rozzano, Milan, Italy. matteo.vecellio@ndorms.ox.ac.uk.ORCID http://orcid.org/0000-0002-8643-1316
Haijing Wu *Hunan Key Laboratory of Medical Epigenomics, Department of Dermatology, The Second Xiangya Hospital, Central South University, #139 Renmin Middle Rd, Changsha, 410011, Hunan, China.
Qianjin Lu *Hunan Key Laboratory of Medical Epigenomics, Department of Dermatology, The Second Xiangya Hospital, Central South University, #139 Renmin Middle Rd, Changsha, 410011, Hunan, China.
Carlo Selmi *Division of Rheumatology and Clinical Immunology, Humanitas Clinical and Research Center, IRCCS, via Manzoni 56, 20089 Rozzano, Milan, Italy.
Central South University · CNHumanitas University · IT

Funding

Ministero degli Affari Esteri e della Cooperazione Internazionale PGR05455Versus Arthritis 21428
6 · The paper itself

Abstract

Genomic predisposition cannot explain the onset of complex diseases, as well illustrated by the largely incomplete concordance among monozygotic twins. Epigenetic mechanisms, including DNA methylation, chromatin remodelling and non-coding RNA, are considered to be the link between environmental stimuli and disease onset on a permissive genetic background in autoimmune and chronic inflammatory diseases. The paradigmatic cases of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), Sjogren's syndrome (SjS) and type-1 diabetes (T1D) share the loss of immunological tolerance to self-antigen influenced by several factors, with a largely incomplete role of individual genomic susceptibility. The most widely investigated epigenetic mechanism is DNA methylation which is associated with gene silencing and is due to the binding of methyl-CpG binding domain (MBD)-containing proteins, such as MECP2, to 5-methylcytosine (5mC). Indeed, a causal relationship occurs between DNA methylation and transcription factors occupancy and recruitment at specific genomic locus. In most cases, the results obtained in different studies are controversial in terms of DNA methylation comparison while fascinating evidence comes from the comparison of the epigenome in clinically discordant monozygotic twins. In this manuscript, we will review the mechanisms of epigenetics and DNA methylation changes in specific immune-mediated rheumatic diseases to highlight remaining unmet needs and to identify possible shared mechanisms beyond different tissue involvements with common therapeutic opportunities. Key Points • DNA methylation has a crucial role in regulating and tuning the immune system. • Evidences suggest that dysregulation of DNA methylation is pivotal in the context of immune-mediated rheumatic diseases. • DNA methylation dysregulation in FOXP3 and interferons-related genes is shared within several autoimmune diseases. • DNA methylation is an attractive marker for diagnosis and therapy.

Indexed as

Autoimmune DiseasesLupus Erythematosus, SystemicRheumatic DiseasesDNA MethylationEpigenesis, GeneticEpigenomicsHumansDNA methylationEpigeneticsRheumatic diseases

Identifiers

PMID32613397
OpenAlexW3040616402

What OpenQuestion holds

Textmetadata
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.