Molecular mechanisms in evolutionary cardiology failure

被引:19
|
作者
Swynghedauw, Bernard [1 ]
Delcayre, Claude
Samuel, Jane-Lyse
Mebazaa, Alexandre [2 ]
Cohen-Solal, Alain [1 ]
机构
[1] Hop Lariboisiere, INSERM, U942, Dept Cardiol, F-75475 Paris 10, France
[2] Hop Lariboisiere, Dept Anesthesiol, F-75475 Paris, France
来源
ANALYSIS OF CARDIAC DEVELOPMENT: FROM EMBRYO TO OLD AGE | 2010年 / 1188卷
关键词
heart failure; cardiac hypertrophy; microRNA; fibrosis; fetal hypothesis; wall stress hypothesis; Laplace's law; aldosterone; evolution; Darwinian or evolutionary medicine; GENE-EXPRESSION; CARDIAC-HYPERTROPHY; HEART-FAILURE; PRESSURE-OVERLOAD; PHENOTYPIC PLASTICITY; ALDOSTERONE; RAT; CARDIOMYOPATHY; TRANSCRIPTOME; MICROARRAY;
D O I
10.1111/j.1749-6632.2009.05084.x
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
Integration of the relevant evolutionary paradigm in cardiology has not yet been fully achieved: In the past, heart failure (HF) was mainly ascribed to infections, and the origins of cardiac hypertrophy (CH) were regarded as mechanical. Recent changes in lifestyle have both reduced the incidence of infections and increased lifespan, and H F is now seen as a complex disease one that is still caused by mechanical disorder, but also associated with ischemia and senescence. The long-held view that CH serves to restore myocardial economy back to normal is still valid. The adaptive process is characterized by a quantitative and a qualitative fetal gene reprogramming, which is now being confirmed by recent advances in microRNA research. It underscores the fact CH is the physiologic reaction of the heart to a pathologic stimulus. The goal for therapy is economic, not inotropic. Another major issue is myocardial fibrosis, a major determinant of diastolic function and arrhythmias. Recent changes in lifestyle have crucially modified the context in which HF occurs.
引用
收藏
页码:58 / 67
页数:10
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