Evidence map›Paper›PMID 37138420›Full record

ReviewCurrent medicinal chemistry2024

The Epigenetic Contribution to the Pathogenesis of Psoriasis: Recent Advances.

Saeed Aslani, Seyed Mohamad Javad Mirarefin, Habib Zarredar, Milad Asadi, Mohammad Reza Javan, Arezou Khosrojerdi, Thomas P Johnston, Amirhossein Sahebkar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current medicinal chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. 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 6 institutions in 4 countries.

Saeed AslaniDepartment of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, VIC 3800, Australia.
Seyed Mohamad Javad MirarefinDepartment of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Habib ZarredarTuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Milad AsadiDepartment of Basic Oncology, Institute of Health Sciences , Ege University, Izmir, Turkey.
Mohammad Reza JavanDepartment of Immunology, Faculty of Medicine, Zabol University of Medical Sciences, Zabol, Iran.
Arezou KhosrojerdiDepartment of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Thomas P JohnstonDivision of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Missouri-Kansas City, Kansas City, MO 64110 , USA.
Amirhossein SahebkarBiotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Tarbiat Modares University · IRMashhad University of Medical Sciences · IREge University · TRHudson Institute of Medical Research · AUTabriz University of Medical Sciences · IRZabol University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is defined as a chronic autoimmune disorder of the skin in which abnormal proliferation and differentiation of keratinocytes are blamed as the central culprit of disease etiopathogenesis. A complex interplay between environmental factors and genetic risk factors has been suggested to trigger the disease. However, epigenetic regulation appears to connect external stimuli and genetic abnormalities in the development of psoriasis. The discordance in the prevalence of psoriasis between monozygotic twins and environmental factors that contribute to its onset have caused a paradigm shift regarding the mechanisms underlying the pathogenesis of this disease. Epigenetic dysregulation may be involved in aberrancies of keratinocyte differentiation, T-cell activation, and other plausible cells, leading to the initiation and perpetuation of psoriasis. Epigenetics is characterized by heritable alterations in the transcription of genes without nucleotide change and is commonly considered at three levels, i.e., DNA methylation, histone modifications, and microRNAs. To date, scientific evidence has indicated abnormal DNA methylation, histone modifications, and non-coding RNA transcription in psoriatic patients. In order to reverse aberrant epigenetic changes in psoriasis patients, several compounds and drugs (epi-drugs) have been developed to affect the major enzymes involved in the methylation of DNA, or the acetylation of histones, which aim to correct the aberrant methylation and acetylation patterns. A number of clinical trials have suggested the therapeutic potential of such drugs in the treatment of psoriasis. In the present review, we attempt to clarify recent findings with respect to epigenetic irregularities in psoriasis and discuss future challenges.

Indexed as

DNA MethylationEpigenesis, GeneticPsoriasisAnimalsHistonesHumansMicroRNAsHistonesMicroRNAsautoimmunityDNA methylationepigeneticshistone modificationsnon-coding RNA.Psoriasis

Identifiers

PMID37138420
OpenAlexW4368356697

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.