Evidence map›Paper›PMID 24310814›Full record

ReviewCellular and molecular life sciences : CMLS2014

Histone deacetylase signaling in cardioprotection.

Lorenz H Lehmann, Barbara C Worst, David A Stanmore, Johannes Backs

Abstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

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  20. Inflammation leads through PGE/EPEMBO molecular medicine · 2018
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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

4 authors.

Lorenz H LehmannResearch Unit Cardiac Epigenetics, Internal Medicine III, Heidelberg University and DZHK (German Center for Cardiovascular Research), partner site Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Barbara C Worst
David A Stanmore
Johannes Backs

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) represents a major challenge for health care systems, both in terms of the high mortality associated with it and the huge economic burden of its treatment. Although CVD represents a diverse range of disorders, they share common compensatory changes in the heart at the structural, cellular, and molecular level that, in the long term, can become maladaptive and lead to heart failure. Treatment of adverse cardiac remodeling is therefore an important step in preventing this fatal progression. Although previous efforts have been primarily focused on inhibition of deleterious signaling cascades, the stimulation of endogenous cardioprotective mechanisms offers a potent therapeutic tool. In this review, we discuss class I and class II histone deacetylases, a subset of chromatin-modifying enzymes known to have critical roles in the regulation of cardiac remodeling. In particular, we discuss their molecular modes of action and go on to consider how their inhibition or the stimulation of their intrinsic cardioprotective properties may provide a potential therapeutic route for the clinical treatment of CVD.

Indexed as

Signal TransductionAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cardiovascular DiseasesHistone Deacetylase InhibitorsHistone DeacetylasesHumansReactive Oxygen SpeciesTranscription FactorsVentricular RemodelingCalcium-Calmodulin-Dependent Protein Kinase Type 2Histone Deacetylase InhibitorsHistone DeacetylasesReactive Oxygen SpeciesTranscription Factors

Identifiers

PMID24310814
PMCPMC3983897

What OpenQuestion holds

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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.