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Givinostat reduces adverse cardiac remodeling through regulating fibroblasts activation.
- Source :
-
Cell death & disease [Cell Death Dis] 2018 Jan 25; Vol. 9 (2), pp. 108. Date of Electronic Publication: 2018 Jan 25. - Publication Year :
- 2018
-
Abstract
- Cardiovascular diseases (CVDs) are a major burden on the healthcare system: indeed, over two million new cases are diagnosed every year worldwide. Unfortunately, important drawbacks for the treatment of these patients derive from our current inability to stop the structural alterations that lead to heart failure, the common endpoint of many CVDs. In this scenario, a better understanding of the role of epigenetics - hereditable changes of chromatin that do not alter the DNA sequence itself - is warranted. To date, hyperacetylation of histones has been reported in hypertension and myocardial infarction, but the use of inhibitors for treating CVDs remains limited. Here, we studied the effect of the histone deacetylase inhibitor Givinostat on a mouse model of acute myocardial infarction. We found that it contributes to decrease endothelial-to-mesenchymal transition and inflammation, reducing cardiac fibrosis and improving heart performance and protecting the blood vessels from apoptosis through the modulatory effect of cardiac fibroblasts on endothelial cells. Therefore, Givinostat may have potential for the treatment of CVDs.
- Subjects :
- Animals
Apoptosis drug effects
Endothelium drug effects
Endothelium pathology
Epithelium drug effects
Epithelium pathology
Female
Fibroblasts drug effects
Fibroblasts metabolism
Fibrosis
Gene Expression Regulation drug effects
Human Umbilical Vein Endothelial Cells drug effects
Human Umbilical Vein Endothelial Cells metabolism
Humans
Inflammation pathology
Mice, Inbred C57BL
Myocardium pathology
Myocytes, Cardiac drug effects
Myocytes, Cardiac pathology
Carbamates pharmacology
Fibroblasts pathology
Ventricular Remodeling drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 2041-4889
- Volume :
- 9
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- Cell death & disease
- Publication Type :
- Academic Journal
- Accession number :
- 29371598
- Full Text :
- https://doi.org/10.1038/s41419-017-0174-5