Evidence map›Paper›PMID 26188466›Full record

ReviewChromosoma2016

Chromatin deregulation in disease.

Anne C Mirabella, Benjamin M Foster, Till Bartke

Open access · hybridAbstract readReview
In one paragraph

Review in Chromosoma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

71 citing papers in PubMed, 137 citations in OpenAlex.

  1. Review
  2. Article
  3. Changing minds epigenetically: Germline genes in neurons disrupt animal behavior.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

11 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

3 authors at 1 institution in 1 country.

Anne C MirabellaChromatin Biochemistry Group, MRC Clinical Sciences Centre, Imperial College London, Du Cane Road, London, W12 0NN, UK.
Benjamin M FosterChromatin Biochemistry Group, MRC Clinical Sciences Centre, Imperial College London, Du Cane Road, London, W12 0NN, UK.
Till BartkeChromatin Biochemistry Group, MRC Clinical Sciences Centre, Imperial College London, Du Cane Road, London, W12 0NN, UK. till.bartke@csc.mrc.ac.uk.
Imperial College London · GB

Funding

Medical Research Council MC_UP_1102/2
6 · The paper itself

Abstract

The regulation of chromatin by epigenetic mechanisms plays a central role in gene expression and is essential for development and maintenance of cell identity and function. Aberrant chromatin regulation is observed in many diseases where it leads to defects in epigenetic gene regulation resulting in pathological gene expression programmes. These defects are caused by inherited or acquired mutations in genes encoding enzymes that deposit or remove DNA and histone modifications and that shape chromatin architecture. Chromatin deregulation often results in neurodevelopmental disorders and intellectual disabilities, frequently linked to physical and developmental abnormalities, but can also cause neurodegenerative diseases, immunodeficiency, or muscle wasting syndromes. Epigenetic diseases can either be of monogenic origin or manifest themselves as complex multifactorial diseases such as in congenital heart disease, autism spectrum disorders, or cancer in which mutations in chromatin regulators are contributing factors. The environment directly influences the epigenome and can induce changes that cause or predispose to diseases through risk factors such as stress, malnutrition or exposure to harmful chemicals. The plasticity of chromatin regulation makes targeting the enzymatic machinery an attractive strategy for therapeutic intervention and an increasing number of small molecule inhibitors against a variety of epigenetic regulators are in clinical use or under development. In this review, we will give an overview of the molecular lesions that underlie epigenetic diseases, and we will discuss the impact of the environment and prospects for epigenetic therapies.

Indexed as

Chromatin Assembly and DisassemblyEpigenesis, GeneticAnimalsAutism Spectrum DisorderChromatinDNAEnvironmental PollutantsFemaleGenetic Predisposition to DiseaseHeart DiseasesHistonesHumansMaleMutationNeoplasmsNeurodegenerative DiseasesChromatinDNAEnvironmental PollutantsHistonesChromatinChromatin remodelingDNA methylationEpigeneticsGene expressionHistone modifications

Identifiers

PMID26188466
PMCPMC4761009
OpenAlexW2157668741

What OpenQuestion 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 OpenQuestion graph.