Inhibition of P38 MAP Kinase Attenuates Left Ventricular Hypertrophy and Inhibits Progression of Systolic Dysfunction on Pressure-Overload Induced Pathological Cardiac Hypertrophy in Mice
スポンサーリンク
概要
- 論文の詳細を見る
Background: P38 mitogen-activated protein kinase(MAP kinase)plays on important role for progression of pathological cardiac hypertrophy. However, the role of p38 MAP kinase in cardiac hypertrophy induced by pressure overload remains unclear. We investigated the effect of chronic treatment with p38 MAP kinase inhibitor on the development of heart failure induced by transverse aortic constriction(TAC)in mice. Methods and Results: TAC increased left ventricular septal wall thickness(LVSWT)and cross-sectional area(CSA)of cardiomyocyte, and decreased LV fractional shortening(FS)compared with sham operation after 6 weeks. TAC also increased phosphorylation of p38 MAP kinase, whereas other hypertrophic signals were unchanged. In another experiment, TAC mice and sham operated mice were treated with subcutaneous injection of p38 MAP kinase inhibitor SB202190(5mg/kg/day)or placebo five times a week for six weeks. Treatment with p38 MAP kinase inhibitor attenuated the increase in LVSWT and CSA, and the decrease in FS in mice with TAC.Conclusions: Inhibition of p38 MAP kinase attenuated left ventricular hypertrophy and inhibited progression of systolic dysfunction in pressure overload-induced cardiac hypertrophy. These results suggest that inhibition of p38 MAP kinase has a protective effect for development of heart failure induced by pressure overload.
- 2011-03-15
論文 | ランダム
- 司会のことば(S10 気道構成細胞から喘息の発症メカニズムを探る,シンポジウム,第60回日本アレルギー学会秋季学術大会)
- 南関東に分布する2.5 Maの広域テフラ: : 丹沢−ざくろ石軽石層
- 大都市近郊における社会関係からみた稲作農家の農地集積形態
- 手術症例報告 腹腔鏡補助下胃全摘後の挙上空腸良性通過障害に対し,磁石圧迫吻合術(山内法)によるρ吻合を行った1例
- 直接形適応制御に基づく適応オブザーバを用いた IPMSM位置センサレス制御の応答改善法