HMGCoA reductase inhibition reverses myocardial fibrosis and diastolic dysfunction through AMP-activated protein kinase activation in a mouse model of metabolic syndrome (vol 99, pg 44, 2013)

Hermida N.

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HMGCoA reductase inhibition reverses myocardial fibrosis and diastolic dysfunction through AMP-activated protein kinase activation in a mouse model of metabolic syndrome (vol 99, pg 44, 2013)

机译：HMGCOA还原酶抑制通过在代谢综合征的小鼠模型中通过AMP活化的蛋白激酶活化来逆转心肌纤维化和舒张功能障碍（Vol 99，PG 44,2013）

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《Cardiovascular Research》 |2021年第4期|共2页
作者
Hermida N.;
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正文语种 eng
中图分类心脏、血管（循环系）疾病;
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1. HMGCoA reductase inhibition reverses myocardial fibrosis and diastolic dysfunction through AMP-activated protein kinase activation in a mouse model of metabolic syndrome [J] . HermidaN., MarklA., HameletJ., Cardiovascular Research . 2013,第1期

机译：HMGCoA还原酶抑制作用通过代谢综合征小鼠模型中的AMP激活的蛋白激酶激活来逆转心肌纤维化和舒张功能障碍
2. Dipeptidyl peptidase inhibition prevents diastolic dysfunction and reduces myocardial fibrosis in a mouse model of Western diet induced obesity [J] . BostickB., HabibiJ., MaL., Metabolism: Clinical and Experimental . 2014,第8期

机译：抑制二肽基肽酶可预防西方饮食诱发肥胖的小鼠模型中的舒张功能障碍并减少心肌纤维化
3. Disturbed cross talk between insulin-like growth factor I and AMP-activated protein kinase as a possible cause of vascular dysfunction in the amyloid precursor protein/presenilin 2 mouse model of Alzheimer's disease. [J] . Lopez-Lopez C, Dietrich MO, Metzger F, The Journal of Neuroscience: The Official Journal of the Society for Neuroscience . 2007,第4期

机译：胰岛素样生长因子I和AMP激活的蛋白激酶之间的干扰干扰是阿尔茨海默氏病的淀粉样蛋白前体蛋白/早老素2小鼠模型中血管功能障碍的可能原因。
4. Dipeptidyl Peptidase Inhibition Prevents Diastolic Dysfunction and Reduces Myocardial Fibrosis in a Mouse Model of Western Diet Induced Obesity [O] . Brian Bostick, Javad Habibi, Lixin Ma, -1

机译：二肽基肽酶抑制作用可预防舒张功能障碍并减少西方饮食诱发肥胖小鼠模型中的心肌纤维化
5. HMGCoA reductase inhibition reverses myocardial fibrosis and diastolic dysfunction through AMP-activated protein kinase activation in a mouse model of metabolic syndrome [O] . Nerea Hermida, Andreas Markl, Julien Hamelet, 2013

机译：HMGCOA还原酶抑制通过在代谢综合征的小鼠模型中通过AMP-活化的蛋白激酶活化逆转心肌纤维化和舒张功能障碍

HMGCoA reductase inhibition reverses myocardial fibrosis and diastolic dysfunction through AMP-activated protein kinase activation in a mouse model of metabolic syndrome (vol 99, pg 44, 2013)

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