Evidence map›Paper›PMID 25759639›Full record

ReviewFrontiers in cellular neuroscience2015

HDAC4 as a potential therapeutic target in neurodegenerative diseases: a summary of recent achievements.

Michal Mielcarek, Daniel Zielonka, Alisia Carnemolla, Jerzy T Marcinkowski, Fabien Guidez

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.8field-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

65 citing papers in PubMed, 112 citations in OpenAlex.

  1. Review
  2. Article
  3. Photoperiod-driven gene regulation in the brain ofFrontiers in endocrinology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Class IIa HDAC4 and HDAC7 cooperatively regulate gene transcription in Th17 cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Tip60's Novel RNA-Binding Function Modulates Alternative Splicing of Pre-mRNA Targets Implicated in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  18. Synthesis and Characterization of Reversible Covalent HDAC4 Inhibitors.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  19. Review
  20. Article

5 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

5 authors at 1 institution in 1 country.

Michal MielcarekDepartment of Medical and Molecular Genetics, King's College London London, UK.
Daniel ZielonkaDepartment of Social Medicine, Poznan University of Medical Sciences Poznan, Poland.
Alisia CarnemollaDepartment of Medical and Molecular Genetics, King's College London London, UK.
Jerzy T MarcinkowskiDepartment of Social Medicine, Poznan University of Medical Sciences Poznan, Poland.
Fabien GuidezINSERM UMRS 1131, Université Paris Diderot, Institut Universitaire d'hématologie (IUH), Hôpital Saint-Louis Paris, France.
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For the past decade protein acetylation has been shown to be a crucial post-transcriptional modification involved in the regulation of protein functions. Histone acetyltransferases (HATs) mediate acetylation of histones which results in the nucleosomal relaxation associated with gene expression. The reverse reaction, histone deacetylation, is mediated by histone deacetylases (HDACs) leading to chromatin condensation followed by transcriptional repression. HDACs are divided into distinct classes: I, IIa, IIb, III, and IV, on the basis of size and sequence homology, as well as formation of distinct repressor complexes. Implications of HDACs in many diseases, such as cancer, heart failure, and neurodegeneration, have identified these molecules as unique and attractive therapeutic targets. The emergence of HDAC4 among the members of class IIa family as a major player in synaptic plasticity raises important questions about its functions in the brain. The characterization of HDAC4 specific substrates and molecular partners in the brain will not only provide a better understanding of HDAC4 biological functions but also might help to develop new therapeutic strategies to target numerous malignancies. In this review we highlight and summarize recent achievements in understanding the biological role of HDAC4 in neurodegenerative processes.

Indexed as

HDAC4HDAC inhibitorshistone deacetylaseneurodegenerationsignalingtherapeutic potential

Identifiers

PMID25759639
PMCPMC4338808
OpenAlexW2043148133

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.