Myocardial infarction mediated by endothelin receptor signaling in hypercholesterolemic mice

被引：134

作者：

Caligiuri, G

Levy, B

Pernow, J

Thorén, P

Hansson, GK ^{[1
]}

机构：

[1] Karolinska Hosp, Ctr Mol Med L803, Dept Med, SE-17176 Stockholm, Sweden

[2] Karolinska Hosp, Cardiol Sect, Dept Med, SE-17176 Stockholm, Sweden

[3] Karolinska Hosp, Ctr Mol Med, Dept Pharmacol & Physiol, SE-17176 Stockholm, Sweden

[4] Hop Lariboisiere, Inst Natl Sante & Rech Med, U141, F-75475 Paris, France

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1999年 / 96卷 / 12期

关键词：

atherosclerosis; cholesterol; gene deletion; hypoxia; stress;

D O I：

10.1073/pnas.96.12.6920

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Myocardial infarction is linked to atherosclerosis, yet the sequence leading from silent coronary atherosclerosis to acute myocardial infarction has remained unclear. Here we show that hypercholesterolemic apolipoprotein E-/- low density lipoprotein receptor(-/-) mice develop not only coronary atherosclerosis but also myocardial infarction, Exposure of mice to mental stress or hypoxia led to acute ischemia, which, in a large proportion of the mice, was followed by electrocardiographic changes, leakage of troponin T, and loss of dehydrogenase from the myocardium, all indicative of acute myocardial infarction, Apoptotic death of cardiomyocytes was followed by inflammation and fibrosis in the heart. All these pathological changes could be prevented by a blocker of the endothelin type A receptor. Thus, stress elicits myocardial infarction through endothelin receptor signaling in coronary atherosclerosis caused by hypercholesterolemia.

引用

页码：6920 / 6924

页数：5

共 41 条

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