ReviewPharmacological reports : PR2026
BET inhibitors in cardiovascular diseases: from atherosclerosis to heart failure.
Review in Pharmacological reports : PR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bromodomain and extra-terminal domain (BET) proteins act as acetyl lysine ‘readers’ that summon transcriptional factors and regulate gene expression. Deregulation of bromodomain-containing protein 4 (BRD4), a transcriptional and epigenetic regulator, is associated with increased epithelial-mesenchymal transition and profibrotic changes in the cardiovascular system. Consistently, BET inhibitors were shown to attenuate cardiac and vascular remodeling induced through several signaling pathways. BRD4 upregulation has been reported in essential hypertension, dyslipidemia, myocardial infarction, heart failure, pulmonary arterial hypertension (PAH), dilated cardiomyopathy, and diabetic cardiomyopathy. Interestingly, BET inhibitors were found to lower blood pressure, downregulate low-density lipoprotein (LDL), oxidative stress markers, and inflammatory cytokine levels, upregulate high-density lipoprotein (HDL), and prevent pathologic cardiac dysfunction and hypertrophy in animal studies. Furthermore, BET inhibition improved heart transplant survival and hindered neointima formation or vascular remodeling in vivo. Moreover, compared to placebo, apabetalone, a selective bromodomain 2 (BD2) inhibitor, improved cardiovascular outcomes in some clinical trials. These promising findings warrant further studies on the efficacy and safety of BET inhibitors for cardiovascular diseases. This review aimed to discuss the efficacy of BET inhibitors for cardiovascular diseases and unravel the underlying mechanisms.
Indexed as
Identifiers
41489727What Socratic holds
Registered trials
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 Socratic graph.