ReviewJournal of molecular and cellular cardiology2014
Targeting cardiac fibroblasts to treat fibrosis of the heart: focus on HDACs.
Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 85 citations in OpenAlex.
- The role of HDAC6 in fibrosis: a novel and effective therapy strategy.European journal of medical research · 2025Review
- Acetylation in Cardiac Aging: Molecular Mechanism and Therapeutic Approaches.Results and problems in cell differentiation · 2025Review
- LMK235 ameliorates inflammation and fibrosis after myocardial infarction by inhibiting LSD1-related pathway.Scientific reports · 2024Article
- High sugar diet-induced fatty acid oxidation potentiates cytokine-dependent cardiac ECM remodeling.The Journal of cell biology · 2024Article
- Fibroblast Diversity and Epigenetic Regulation in Cardiac Fibrosis.International journal of molecular sciences · 2024Review
- Possible organ-protective effects of renal denervation: insights from basic studies.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Review
- The Role of Selected Epigenetic Pathways in Cardiovascular Diseases as a Potential Therapeutic Target.International journal of molecular sciences · 2023Review
- Cytokine receptor-like factor 1 (CRLF1) promotes cardiac fibrosis via ERK1/2 signaling pathway.Journal of Zhejiang University. Science. B · 2023Article
- Myofibroblast specific targeting approaches to improve fibrosis treatment.Chemical communications (Cambridge, England) · 2022Review
- Review
- Matrix-Degrading Enzyme Expression and Aortic Fibrosis During Continuous-Flow Left Ventricular Mechanical Support.Journal of the American College of Cardiology · 2021Article
- Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities.Advanced drug delivery reviews · 2021Review
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Diabetic fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- RNA-Binding Profiles of CKAP4 as an RNA-Binding Protein in Myocardial Tissues.Frontiers in cardiovascular medicine · 2021Article
- Histone Deacetylases in the Pathogenesis of Diabetic Cardiomyopathy.Frontiers in endocrinology · 2021Review
- Overexpression of peptidase inhibitor 16 attenuates angiotensin II-induced cardiac fibrosis via regulating HDAC1 of cardiac fibroblasts.Journal of cellular and molecular medicine · 2020Article
- Article
- Dynamic Chromatin Targeting of BRD4 Stimulates Cardiac Fibroblast Activation.Circulation research · 2019Article
- Improved Selective Class I HDAC and Novel Selective HDAC3 Inhibitors: Beyond Hydroxamic Acids and Benzamides.ACS medicinal chemistry letters · 2019Article
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
Abstract
Cardiac fibrosis is implicated in numerous physiologic and pathologic conditions, including scar formation, heart failure and cardiac arrhythmias. However the specific cells and signaling pathways mediating this process are poorly understood. Lysine acetylation of nucleosomal histone tails is an important mechanism for the regulation of gene expression. Additionally, proteomic studies have revealed that thousands of proteins in all cellular compartments are subject to reversible lysine acetylation, and thus it is becoming clear that this post-translational modification will rival phosphorylation in terms of biological import. Acetyl groups are conjugated to lysine by histone acetyltransferases (HATs) and removed from lysine by histone deacetylases (HDACs). Recent studies have shown that pharmacologic agents that alter lysine acetylation by targeting HDACs have the remarkable ability to block pathological fibrosis. Here, we review the current understanding of cardiac fibroblasts and the fibrogenic process with respect to the roles of lysine acetylation in the control of disease-related cardiac fibrosis. Potential for small molecule HDAC inhibitors as anti-fibrotic therapeutics that target cardiac fibroblasts is highlighted. This article is part of a Special Issue entitled "Myocyte-Fibroblast Signalling in Myocardium."
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.