@article{oai:hirosaki.repo.nii.ac.jp:00003720,
 author = {Hanada, Kenji and Osanai, Tomohiro and Sukekawa, Takanori and Ohya, Fumie and Izumiyama, Kei and Sagara, Shigeki and Itoh, Taihei and Yamamoto, Yuko and Shibutani, Shuji and Tomita, Hirofumi and Okumura, Ken},
 issue = {1},
 journal = {弘前医学},
 month = {Mar},
 note = {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., 弘前医学. 62(1), 2011, p.18-26},
 pages = {18--26},
 title = {Inhibition of P38 MAP Kinase Attenuates Left Ventricular Hypertrophy and Inhibits Progression of Systolic Dysfunction on Pressure-Overload Induced Pathological Cardiac Hypertrophy in Mice},
 volume = {62},
 year = {2011}
}