Evidence map›Paper›PMID 28856178›Full record

ReviewBone reports2017

Histone deacetylases and their roles in mineralized tissue regeneration.

Nam Cong-Nhat Huynh, Vincent Everts, Ruchanee Salingcarnboriboon Ampornaramveth

Open access · goldAbstract readReview
In one paragraph

Review in Bone reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Myc beyond Cancer: Regulation of Mammalian Tissue Regeneration.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Review
  10. Regulation of chromatin organization during animal regeneration.Cell regeneration (London, England) · 2023
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Multiple ways for the same destination: bone regeneration.Maxillofacial plastic and reconstructive surgery · 2022
    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

3 authors at 3 institutions in 3 countries.

Nam Cong-Nhat HuynhDepartment of Dental Basic Sciences, Faculty of Odonto-Stomatology, University of Medicine and Pharmacy at Ho Chi Minh City, Viet Nam.
Vincent EvertsDepartment of Oral Cell Biology, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and Vrije Universiteit Amsterdam, Research Institute MOVE, Gustav Mahlerlaan 3004, 1081 LA Amsterdam, The Netherlands.
Ruchanee Salingcarnboriboon AmpornaramvethResearch Unit on Oral Microbiology and Immunology, Microbiology Department, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand.
Academic Center for Dentistry Amsterdam · NLChulalongkorn University · THHo Chi Minh City Medicine and Pharmacy University · VN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone acetylation is an important epigenetic mechanism that controls expression of certain genes. It includes non-sequence-based changes of chromosomal regional structure that can alter the expression of genes. Acetylation of histones is controlled by the activity of two groups of enzymes: the histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDACs remove acetyl groups from the histone tail, which alters its charge and thus promotes compaction of DNA in the nucleosome. HDACs render the chromatin structure into a more compact form of heterochromatin, which makes the genes inaccessible for transcription. By altering the transcriptional activity of bone-associated genes, HDACs control both osteogenesis and osteoclastogenesis. This review presents an overview of the function of HDACs in the modulation of bone formation. Special attention is paid to the use of HDAC inhibitors in mineralized tissue regeneration from cells of dental origin.

Indexed as

ADSCs, adipose tissue-derived stem cellsALP, alkaline phosphataseBone regenerationBSP, bone sialoproteinCOL1, type I collagenDentin formationDMP1, dentin matrix acidic phosphoprotein 1DPSCs, dental-derived stem cellsDSPP, dentin sialophosphoproteinEpigeneticGSK-3, glycogen synthase kinaseHAT, histone acetyltransferaseHDAC, histone deacetylaseHistone acetyltransferaseHistone deacetylasehPDLCs, human periodontal ligament cellsMSCs, mesenchymal stem cellsNaB, sodium butyrateOCN, osteocalcinOPN, osteopontinPCL/PEG, polycaprolactone/polyethylene glycolRUNX2, runt-related transcription factor 2SOST, sclerostinTGF-β/BMP, transforming growth factor-β/bone morphogenetic proteinTSA, Trichostatin AVPA, valproic acidWNT/β-catenin, Wingless-int

Identifiers

PMID28856178
PMCPMC5565747
OpenAlexW2748484626

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.