Evidence map›Paper›PMID 37461108›Full record

ReviewJournal of translational medicine2023

Unraveling the epigenetic landscape of pulmonary arterial hypertension: implications for personalized medicine development.

Jaydev Dave, Vineeta Jagana, Radoslav Janostiak, Malik Bisserier

Open access · goldAbstract readReview
In one paragraph

Review in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
10.9field-weighted citation impact, top 1% 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

37 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. A Paradigm Shift of HCurrent issues in molecular biology · 2026
    Review
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  9. Current Evidence on the Potential Role of EndothelialReviews in cardiovascular medicine · 2026
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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 at 2 institutions in 2 countries.

Jaydev DaveDepartment of Cell Biology and Anatomy, New York Medical College, 15 Dana Road, BSB 131A, Valhalla, NY, 10595, USA.
Vineeta JaganaDepartment of Cell Biology and Anatomy, New York Medical College, 15 Dana Road, BSB 131A, Valhalla, NY, 10595, USA.
Radoslav JanostiakFirst Faculty of Medicine, BIOCEV, Charles University, Vestec, 25250, Czech Republic.
Malik BisserierDepartment of Cell Biology and Anatomy, New York Medical College, 15 Dana Road, BSB 131A, Valhalla, NY, 10595, USA. mbisseri@nymc.edu.ORCID 0000-0001-8826-4649
New York Medical College · USCharles University · CZ

Funding

PRIDE Academy: Impact of Ancestry and Gender to omics of lung diseasesR25HL146166 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Matthew Wayne DeCamp, Sonia Castro Flores · 2019 to 2026
$3.4M
Role of SIN3a in the epigenetic regulation of the Bone Morphogenetic Protein Receptor Type 2 in pulmonary arterial hypertensionK01HL159038 · NHLBI · NEW YORK MEDICAL COLLEGE · PI BISSERIER, MALIK · 2022 to 2024
$406k
NHLBI NIH HHS 1K01HL159038NHLBI NIH HHS 5R25HL146166NHLBI NIH HHS R25 HL146166
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a multifactorial disease associated with the remodeling of pulmonary blood vessels. If left unaddressed, PAH can lead to right heart failure and even death. Multiple biological processes, such as smooth muscle proliferation, endothelial dysfunction, inflammation, and resistance to apoptosis, are associated with PAH. Increasing evidence suggests that epigenetic factors play an important role in PAH by regulating the chromatin structure and altering the expression of critical genes. For example, aberrant DNA methylation and histone modifications such as histone acetylation and methylation have been observed in patients with PAH and are linked to vascular remodeling and pulmonary vascular dysfunction. In this review article, we provide a comprehensive overview of the role of key epigenetic targets in PAH pathogenesis, including DNA methyltransferase (DNMT), ten-eleven translocation enzymes (TET), switch-independent 3A (SIN3A), enhancer of zeste homolog 2 (EZH2), histone deacetylase (HDAC), and bromodomain-containing protein 4 (BRD4). Finally, we discuss the potential of multi-omics integration to better understand the molecular signature and profile of PAH patients and how this approach can help identify personalized treatment approaches.

Indexed as

Hypertension, PulmonaryPulmonary Arterial HypertensionBromodomain Containing ProteinsCell Cycle ProteinsEpigenesis, GeneticHumansNuclear ProteinsPrecision MedicinePulmonary ArteryTranscription FactorsVascular RemodelingBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsNuclear ProteinsTranscription FactorsEpidrugsEpigeneticPAHPulmonary arterial hypertensionTreatment

Identifiers

PMID37461108
PMCPMC10353122
OpenAlexW4384559892

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.