ReviewMolecular and cellular biochemistry2025
Unlocking cardiac health: exploring the role of class I HDACs in cardiovascular diseases.
Review in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- The Trajectory of Epigenetic Chromatin Remodeling in Cardiometabolic Disease and its Therapeutic Implications.Journal of cardiovascular translational research · 2026Review
- Molecular Mechanisms of Cardiac Fibrosis: A Pathologist's Perspective.Current issues in molecular biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Translation modifications, particularly those involving histone deacetylases (HDACs), are crucial for regulating gene expression and have significant implications for cardiovascular disease (CVD). The association between HDACs and CVD has garnered significant research interest due to the pivotal role of HDACs in gene expression regulation and cellular function. Aberrant HDAC activity has been implicated in various pathological processes underlying CVD, including inflammation, endothelial dysfunction, hypertrophy, fibrosis, and atherosclerosis. This review explores the molecular mechanisms by which different HDAC isoforms influence cardiovascular pathology, highlighting evidence from preclinical and clinical studies. Emerging data suggest that HDAC inhibitors could offer therapeutic potential by modulating these processes and improving cardiovascular health. However, the precise isoform-specific roles and therapeutic window for HDAC inhibition in CVD remain to be elucidated. Furthermore, research is essential to identify the crucial and complex relationship between HDACs and cardiovascular health, which could pave the way for novel, targeted interventions for the treatment of CVD.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.