Evidence map›Paper›PMID 19583816›Full record

ReviewJournal of cellular and molecular medicine2009

Histone deacetylase inhibition and the regulation of cell growth with particular reference to liver pathobiology.

Fraczek Joanna, Leo A van Grunsven, Vinken Mathieu, Snykers Sarah, Deleu Sarah, Vanderkerken Karin, Vanhaecke Tamara, Rogiers Vera

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025
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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 1 institution in 1 country.

Fraczek JoannaDepartment of Toxicology, Vrije Universiteit Brussel, Laarbeeklaan, Brussels, Belgium. jfraczek@vub.ac.be
Leo A van Grunsven
Vinken Mathieu
Snykers Sarah
Deleu Sarah
Vanderkerken Karin
Vanhaecke Tamara
Rogiers Vera
Vrije Universiteit Brussel · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcriptional activity of genes largely depends on the accessibility of specific chromatin regions to transcriptional regulators. This process is controlled by diverse post-transcriptional modifications of the histone amino termini of which reversible acetylation plays a vital role. Histone acetyltransferases (HATs) are responsible for the addition of acetyl groups and histone deacetylases (HDACs) catalyse the reverse reaction. In general, though not exclusively, histone acetylation is associated with a positive regulation of transcription, whereas histone deacetylation is correlated with transcriptional silencing. The elucidation of unequivocal links between aberrant action of HDACs and tumorigenesis lies at the base of key scientific importance of these enzymes. In particular, the potential benefit of HDAC inhibition has been confirmed in various tumour cell lines, demonstrating antiproliferative, differentiating and pro-apoptotic effects. Consequently, the dynamic quest for HDAC inhibitors (HDIs) as a new class of anticancer drugs was set off, resulting in a number of compounds that are currently evaluated in clinical trials. Ironically, the knowledge with respect to the expression pattern and function of individual HDAC isoenzymes remains largely elusive. In the present review, we provide an update of the current knowledge on the involvement of HDACs in the regulation of fundamental cellular processes in the liver, being the main site for drug metabolism within the body. Focus lies on the involvement of HDACs in the regulation of growth of normal and transformed hepatocytes and the transdifferentiation process of stellate cells. Furthermore, extrapolation of our present knowledge on HDAC functionality towards innovative treatment of malignant and non-malignant, hyperproliferative and inflammatory disorders is discussed.

Indexed as

AnimalsCarcinoma, HepatocellularCell ProliferationCyclin-Dependent Kinase Inhibitor p21FibrosisHepatocytesHistone Deacetylase InhibitorsHistone DeacetylasesHistonesHumansInflammationLiverModels, BiologicalRetinoblastomaTumor Suppressor Protein p53CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Histone Deacetylase InhibitorsHistone DeacetylasesHistonesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID19583816
PMCPMC4516460
OpenAlexW2050331458

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.