Effects of Pitavastatin on Pressure Overload-Induced Heart Failure in Mice
Background: 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammato...
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| Published in | Circulation Journal Vol. 76; no. 5; pp. 1159 - 1168 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Japan
The Japanese Circulation Society
2012
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1346-9843 1347-4820 1347-4820 |
| DOI | 10.1253/circj.CJ-11-1114 |
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| Abstract | Background: 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammatory effect. It is unclear, however, whether statins have any effects on the progression from left ventricular (LV) hypertrophy to heart failure in the established hypertrophied heart. Methods and Results: C57BL/6 mice were treated with pitavastatin (pitava) or vehicle (control) from 2 weeks (established hypertrophy stage) after transverse aortic constriction (TAC) and the treatment was continued for 4 weeks. Pitavastatin significantly inhibited the progression from LV hypertrophy to heart failure as assessed on echocardiography. The cardiomyocyte cross-sectional area was significantly increased in the control group compared to the sham-operated mice (sham group), but it was not significantly different between the control group and the pitava group at 6 weeks after TAC. Moreover, pitavastatin induced myocardial angiogenesis (ratio of number of endothelial cells to cardiomyocytes) and decreased the myocardial fibrosis and oxidative stress. The expression of angiopoietin-1 in the heart was significantly increased by pitavastatin at 6 weeks after TAC. Conclusions: Pitavastatin has preventive effects on the progression of heart failure even in the hypertrophied heart. (Circ J 2012; 76: 1159-1168) |
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| AbstractList | 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammatory effect. It is unclear, however, whether statins have any effects on the progression from left ventricular (LV) hypertrophy to heart failure in the established hypertrophied heart.
C57BL/6 mice were treated with pitavastatin (pitava) or vehicle (control) from 2 weeks (established hypertrophy stage) after transverse aortic constriction (TAC) and the treatment was continued for 4 weeks. Pitavastatin significantly inhibited the progression from LV hypertrophy to heart failure as assessed on echocardiography. The cardiomyocyte cross-sectional area was significantly increased in the control group compared to the sham-operated mice (sham group), but it was not significantly different between the control group and the pitava group at 6 weeks after TAC. Moreover, pitavastatin induced myocardial angiogenesis (ratio of number of endothelial cells to cardiomyocytes) and decreased the myocardial fibrosis and oxidative stress. The expression of angiopoietin-1 in the heart was significantly increased by pitavastatin at 6 weeks after TAC.
Pitavastatin has preventive effects on the progression of heart failure even in the hypertrophied heart. Background: 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammatory effect. It is unclear, however, whether statins have any effects on the progression from left ventricular (LV) hypertrophy to heart failure in the established hypertrophied heart. Methods and Results: C57BL/6 mice were treated with pitavastatin (pitava) or vehicle (control) from 2 weeks (established hypertrophy stage) after transverse aortic constriction (TAC) and the treatment was continued for 4 weeks. Pitavastatin significantly inhibited the progression from LV hypertrophy to heart failure as assessed on echocardiography. The cardiomyocyte cross-sectional area was significantly increased in the control group compared to the sham-operated mice (sham group), but it was not significantly different between the control group and the pitava group at 6 weeks after TAC. Moreover, pitavastatin induced myocardial angiogenesis (ratio of number of endothelial cells to cardiomyocytes) and decreased the myocardial fibrosis and oxidative stress. The expression of angiopoietin-1 in the heart was significantly increased by pitavastatin at 6 weeks after TAC. Conclusions: Pitavastatin has preventive effects on the progression of heart failure even in the hypertrophied heart. (Circ J 2012; 76: 1159-1168) 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammatory effect. It is unclear, however, whether statins have any effects on the progression from left ventricular (LV) hypertrophy to heart failure in the established hypertrophied heart.BACKGROUND3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have various pleiotropic effects such as protective effect of endothelial cells, angiogenic effect, antioxidant effect and anti-inflammatory effect. It is unclear, however, whether statins have any effects on the progression from left ventricular (LV) hypertrophy to heart failure in the established hypertrophied heart.C57BL/6 mice were treated with pitavastatin (pitava) or vehicle (control) from 2 weeks (established hypertrophy stage) after transverse aortic constriction (TAC) and the treatment was continued for 4 weeks. Pitavastatin significantly inhibited the progression from LV hypertrophy to heart failure as assessed on echocardiography. The cardiomyocyte cross-sectional area was significantly increased in the control group compared to the sham-operated mice (sham group), but it was not significantly different between the control group and the pitava group at 6 weeks after TAC. Moreover, pitavastatin induced myocardial angiogenesis (ratio of number of endothelial cells to cardiomyocytes) and decreased the myocardial fibrosis and oxidative stress. The expression of angiopoietin-1 in the heart was significantly increased by pitavastatin at 6 weeks after TAC.METHODS AND RESULTSC57BL/6 mice were treated with pitavastatin (pitava) or vehicle (control) from 2 weeks (established hypertrophy stage) after transverse aortic constriction (TAC) and the treatment was continued for 4 weeks. Pitavastatin significantly inhibited the progression from LV hypertrophy to heart failure as assessed on echocardiography. The cardiomyocyte cross-sectional area was significantly increased in the control group compared to the sham-operated mice (sham group), but it was not significantly different between the control group and the pitava group at 6 weeks after TAC. Moreover, pitavastatin induced myocardial angiogenesis (ratio of number of endothelial cells to cardiomyocytes) and decreased the myocardial fibrosis and oxidative stress. The expression of angiopoietin-1 in the heart was significantly increased by pitavastatin at 6 weeks after TAC.Pitavastatin has preventive effects on the progression of heart failure even in the hypertrophied heart.CONCLUSIONSPitavastatin has preventive effects on the progression of heart failure even in the hypertrophied heart. |
| Author | Kameda, Yoshihito Hasegawa, Hiroshi Takano, Hiroyuki Kobayashi, Yoshio Kubota, Akihiko Tadokoro, Hiroyuki Komuro, Issei |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22361916$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1161_CIRCRESAHA_114_300507 crossref_primary_10_1016_j_bcp_2019_06_018 crossref_primary_10_1253_circj_CJ_12_0722 crossref_primary_10_1016_j_jphs_2017_11_006 crossref_primary_10_1536_ihj_21_231 crossref_primary_10_1038_hr_2016_122 crossref_primary_10_1097_HJH_0000000000002728 crossref_primary_10_18678_dtfd_1435020 crossref_primary_10_1038_srep43920 crossref_primary_10_1016_j_bbadis_2016_05_019 crossref_primary_10_3892_mmr_2013_1548 crossref_primary_10_1016_j_ncrna_2017_01_001 crossref_primary_10_1161_HYPERTENSIONAHA_115_07089 crossref_primary_10_1038_hr_2015_141 |
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| Snippet | Background: 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported... 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), which are widely used to lower plasma cholesterol levels, have been reported to have... |
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| SubjectTerms | Angiogenesis Angiopoietin-1 - biosynthesis Animals Blood Pressure Cardiac fibrosis Fibrosis - etiology Fibrosis - metabolism Fibrosis - pathology Fibrosis - prevention & control Gene Expression Regulation - drug effects Heart failure Heart Failure - etiology Heart Failure - metabolism Heart Failure - pathology Heart Failure - prevention & control HMG-CoA reductase inhibitor Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology Hypertrophy, Left Ventricular - complications Hypertrophy, Left Ventricular - metabolism Hypertrophy, Left Ventricular - pathology Left ventricular hypertrophy Mice Myocardium - metabolism Myocardium - pathology Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - pathology Neovascularization, Pathologic - prevention & control Oxidative Stress - drug effects Quinolines - pharmacokinetics Time Factors |
| Title | Effects of Pitavastatin on Pressure Overload-Induced Heart Failure in Mice |
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