Myocardial stress and hypertrophy: a complex interface between biophysics and cardiac remodeling
Myocardial stress and hypertrophy: a complex interface between biophysics and cardiac remodeling
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DOI：
10.1172/jci69830
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发表时间：
2013-09-01
影响因子：
15.9
通讯作者：
Paulus, Walter J.
中科院分区：
文献类型：
--
作者：
Grossman, William;Paulus, Walter J.
压力和容量超负荷导致心室腔向心性和离心性肥大，分别具有平行和串联复制的肌节。40年前，这些不同的肥大模式与两种情况下不同的壁应力有关，收缩期壁应力引起肌节的平行复制，舒张期壁应力引起肌节的串联复制。这些观察结果与临床实践相关，因为它们与主动脉瓣狭窄患者中经常观察到的过度肥大和收缩功能障碍有关。心肌细胞的应力感应机制和心肌细胞死亡的激活，提高壁应力继续感兴趣的心血管科学家。
Pressure and volume overload results in concentric and eccentric hypertrophy of cardiac ventricular chambers with, respectively, parallel and series replication of sarcomeres. These divergent patterns of hypertrophy were related 40 years ago to disparate wall stresses in both conditions, with systolic wall stress eliciting parallel replication of sarcomeres and diastolic wall stress, series replication. These observations are relevant to clinical practice, as they relate to the excessive hypertrophy and contractile dysfunction regularly observed in patients with aortic stenosis. Stress-sensing mechanisms in cardiomyocytes and activation of cardiomyocyte death by elevated wall stress continue to intrigue cardiovascular scientists.