mortality/aging
|
• after tamoxifen (TMX) treatment, mice exhibit significantly enhanced survival relative to Mtortm1.1Gcon/Mtortm1.1Gcon A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice
|
cardiovascular system
|
• at 4 weeks after TMX treatment, mice exhibit normal echocardiographic parameters, cardiomyocyte size, and cardiac function (as assessed by the LV fractional shortening %)
|
|
• at 4 weeks after TMX treatment, mice show significantly reduced fibrosis relative to Mtortm1.1Gcon/Mtortm1.1Gcon A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice
|
cellular
|
• at 4 weeks after TMX treatment, mice show significantly reduced fibrosis relative to Mtortm1.1Gcon/Mtortm1.1Gcon A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice
|
|
• after TMX treatment, mice show a similar expression of autophagy genes relative to Mtortm1.1Gcon/Mtortm1.1Gcon A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice, suggesting that autophagy is not involved in the amelioration of the heart failure phenotype
|
|
• at 4 weeks after TMX treatment, mice show a significant decrease of cleaved Parp protein and TUNEL+ cells in the myocardium relative to Mtortm1.1Gcon/Mtortm1.1Gcon A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice
|
|
• at 4 weeks after TMX treatment, mice show increased cytochrome c oxidase subunit IV (CoxIV) expression in heart lysates relative to Mtortm1.1Gcon/Mtortm1.1Gcon A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice, suggesting that mitochondrial function is improved
|
muscle
|
• at 4 weeks after TMX treatment, mice show a significant decrease of cleaved Parp protein and TUNEL+ cells in the myocardium relative to Mtortm1.1Gcon/Mtortm1.1Gcon A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice
|
homeostasis/metabolism
|
• after TMX treatment, mice show a similar expression of autophagy genes relative to Mtortm1.1Gcon/Mtortm1.1Gcon A1cfTg(Myh6-cre/Esr1*)1Jmk/0 mice, suggesting that autophagy is not involved in the amelioration of the heart failure phenotype
|