Evidence map›Paper›PMID 35699165›Full record

ArticleJournal of the American Heart Association2022

Histone Deacetylase 6 Inhibitor JS28 Prevents Pathological Gene Expression in Cardiac Myocytes.

Vivien Ngo, Bernd K Fleischmann, Manfred Jung, Lutz Hein, Achim Lother

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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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

5 authors at 2 institutions in 1 country.

Vivien NgoInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine University of Freiburg Germany.ORCID 0000-0002-3079-8418
Bernd K FleischmannInstitute of Physiology I, Life & Brain Center, Medical Faculty University of Bonn Germany.ORCID 0000-0002-9202-8363
Manfred JungInstitute of Pharmaceutical Sciences University of Freiburg Germany.ORCID 0000-0002-6361-7716
Lutz HeinInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine University of Freiburg Germany.ORCID 0000-0003-1297-0007
Achim LotherInstitute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine University of Freiburg Germany.ORCID 0000-0001-9107-5558
University of Freiburg · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background Epigenetic modulators have been proposed as promising new drug targets to treat adverse remodeling in heart failure. Here, we evaluated the potential of 4 epigenetic drugs, including the recently developed histone deacetylase 6 (HDAC6) inhibitor JS28, to prevent endothelin-1 induced pathological gene expression in cardiac myocytes and analyzed the chromatin binding profile of the respective inhibitor targets. Methods and Results Cardiac myocytes were differentiated and puromycin-selected from mouse embryonic stem cells and treated with endothelin-1 to induce pathological gene expression (938 differentially expressed genes, q<0.05). Dysregulation of gene expression was at least in part prevented by epigenetic inhibitors, including the pan-BRD (bromodomain-containing protein) inhibitor bromosporine (290/938 genes), the BET (bromodomain and extraterminal) inhibitor JQ1 (288/938), the broad-spectrum HDAC inhibitor suberoylanilide hydroxamic acid (227/938), and the HDAC6 inhibitor JS28 (210/938). Although the 4 compounds were similarly effective toward pathological gene expression, JS28 demonstrated the least adverse effects on physiological gene expression. Genome-wide chromatin binding profiles revealed that HDAC6 binding sites were preferentially associated with promoters of genes involved in RNA processing. In contrast, BRD4 binding was associated with genes involved in core cardiac myocyte functions, for example, myocyte contractility, and showed enrichment at enhancers and intronic regions. These distinct chromatin binding profiles of HDAC6 and BRD4 might explain the different effects of their inhibitors on pathological versus physiological gene expression. Conclusions In summary, we demonstrated, that the HDAC6 inhibitor JS28 effectively prevented the adverse effects of endothelin-1 on gene expression with minor impact on physiological gene expression in cardiac myocytes. Selective HDAC6 inhibition by JS28 appears to be a promising strategy for future evaluation in vivo and potential translation into clinical application.

Indexed as

Histone Deacetylase InhibitorsMyocytes, CardiacAnimalsChromatinEndothelin-1Gene ExpressionHistone Deacetylase 6MiceNuclear ProteinsTranscription FactorsChromatinEndothelin-1Histone Deacetylase 6Histone Deacetylase InhibitorsNuclear ProteinsTranscription Factorsbromodomain‐containing proteincardiac myocyteepigeneticsheartheart failurehistone deacetylase

Identifiers

PMID35699165
PMCPMC9238633
OpenAlexW4282827709

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.