ReviewMolecular medicine reports2018
Cell‑specific histone modifications in atherosclerosis (Review).
Review in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 39 citations in OpenAlex.
- The Future of Epigenetics: Emerging Technologies and Clinical Applications.ACS pharmacology & translational science · 2026Review
- Review
- Epigenetic Regulation and Molecular Mechanisms in Cardiovascular Diseases: A Review of Recent Advances and Therapeutic Implications.International journal of molecular sciences · 2026Review
- HDAC6 deficiency exacerbates atherosclerosis via STAT3-K685 acetylation-mediated CD36/SR-A upregulation in macrophages.Cell death & disease · 2025Article
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- Common Pathophysiological Mechanisms Connecting Dyslipidemia and Hyperuricemia: a Narrative Review.Maedica · 2025Review
- Genomic and Precision Medicine Approaches in Atherosclerotic Cardiovascular Disease: From Risk Prediction to Therapy-A Review.Biomedicines · 2025Review
- Review
- Computational Biology in the Discovery of Biomarkers in the Diagnosis, Treatment and Management of Cardiovascular Diseases.Cardiology and cardiovascular medicine · 2024Article
- Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024Review
- DNA methylation and histone post-translational modifications in atherosclerosis and a novel perspective for epigenetic therapy.Cell communication and signaling : CCS · 2023Review
- Nuclear mechanosensing of the aortic endothelium in health and disease.Disease models & mechanisms · 2023Review
- LSD1 for the Targeted Regulation of Adipose Tissue.Current issues in molecular biology · 2022Review
- Pharmacological Inhibition of Lysine-Specific Demethylase 1A Reduces Atherosclerotic Lesion Formation in Apolipoprotein E-Deficient Mice by a Mechanism Involving Decreased Oxidative Stress and Inflammation; Potential Implications in Human Atherosclerosis.Antioxidants (Basel, Switzerland) · 2022Article
- The Epigenome in Atherosclerosis.Handbook of experimental pharmacology · 2022Article
- Histone Deacetylase9 Represents the Epigenetic Promotion of M1 Macrophage Polarization and Inflammatory Response via TLR4 Regulation.BioMed research international · 2022Article
- Development of necroptosis-related gene signature to predict the prognosis of colon adenocarcinoma.Frontiers in genetics · 2022Article
- Article
- Epigenetic Regulation of Endothelial Cell Function by Nucleic Acid Methylation in Cardiac Homeostasis and Disease.Cardiovascular drugs and therapy · 2021Review
- Pharmacological inhibition of EZH2 by GSK126 decreases atherosclerosis by modulating foam cell formation and monocyte adhesion in apolipoprotein E-deficient mice.Experimental and therapeutic medicine · 2021Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone modifications are the key epigenetic mechanisms that have been identified to regulate gene expression in many human diseases. However, in the early developmental stages, such as in utero and the postnatal stages, histone modifications are essential for gene regulation and cell growth. Atherosclerosis represents a classical example of the involvement of different cell types, and their cumulative effects in the development of atheroma and the progression of the disease. Post translational modifications on proteins either induces their functional activity or renders them inactive. Post translational modifications such as methylation or acetylation on histones have been well characterized, and their role in enhancing or inhibiting specific gene expression was clearly elucidated. In the present review article, the critical roles of different histone modifications that occur in atherosclerosis have been summarized. Different histone proteins have been identified to serve a critical role in the development of atherosclerosis. Specifically, histone methylation and histone acetylation in monocytes, macrophages, vascular smooth muscle cells and in endothelial cells during the progression of atherosclerosis, have been well reported. In recent years, different target molecules and genes that regulate histone modifications have been examined for their effects in the treatment of atherosclerosis in animal models and in clinical trials. An increasing body of evidence suggests that these epigenetic changes resulting from DNA methylation and non‑coding RNA may also be associated with histone modifications, thereby indicating that novel therapeutic strategies can be developed by targeting these post translational modifications, which may in turn aid in the treatment of atherosclerosis.
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.