TY - JOUR
T1 - Givinostat reduces adverse cardiac remodeling through regulating fibroblasts activation article
AU - Milan, Marika
AU - Pace, Valentina
AU - Maiullari, Fabio
AU - Chirivì, Maila
AU - Baci, Denisa
AU - Maiullari, Silvia
AU - Madaro, Luca
AU - Maccari, Sonia
AU - Stati, Tonino
AU - Marano, Giuseppe
AU - Frati, Giacomo
AU - Puri, Pier Lorenzo
AU - De Falco, Elena
AU - Bearzi, Claudia
AU - Rizzi, Roberto
PY - 2017/11/13
Y1 - 2017/11/13
N2 - 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.
AB - 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.
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U2 - 10.1038/s41419-017-0174-5
DO - 10.1038/s41419-017-0174-5
M3 - Article
AN - SCOPUS:85041100911
VL - 9
JO - Cell Death and Disease
JF - Cell Death and Disease
SN - 2041-4889
IS - 2
M1 - 108
ER -