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首页> 外文期刊>Acta biomaterialia >Computational modeling of cardiac growth and remodeling in pressure overloaded hearts-Linking microstructure to organ phenotype
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Computational modeling of cardiac growth and remodeling in pressure overloaded hearts-Linking microstructure to organ phenotype

机译：心脏生长和压力重塑的计算建模超载心脏链接微观结构与器官表型

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Cardiac growth and remodeling (G&R) refers to structural changes in myocardial tissue in response to chronic alterations in loading conditions. One such condition is pressure overload where elevated wall stresses stimulate the growth in cardiomyocyte thickness, associated with a phenotype of concentric hypertrophy at the organ scale, and promote fibrosis. The initial hypertrophic response can be considered adaptive and beneficial by favoring myocyte survival, but over time if pressure overload conditions persist, maladaptive mechanisms favoring cell death and fibrosis start to dominate, ultimately mediating the transition towards an overt heart failure phenotype. The underlying mechanisms linking biological factors at the myocyte level to biomechanical factors at the systemic and organ level remain poorly understood. Computational models of G&R show high promise as a unique framework for providing a quantitative link between myocardial stresses and strains at the organ scale to biological regulatory processes at the cellular level which govern the hypertrophic response. However, microstructurally motivated, rigorously validated computational models of G&R are still in their infancy.
机译：心脏生长和重塑（G＆R）是指心肌组织的结构变化，响应于负载条件的慢性改变。一种这样的条件是压力过载，其中升高的壁应力刺激心肌细胞厚度的生长，与器官尺度的同心肥厚表型相关，促进纤维化。初始肥厚反应可以通过青睐肌细胞存活，但随着时间的推移，如果压力过载条件持续存在，有利于细胞死亡和纤维化的不良机制开始占据主导地位，最终将过渡到公开的心力衰竭表型。将生物细胞水平与系统和器官水平的生物力学因子联系起来的潜在机制仍然明白。 G＆R的计算模型显示出高度应该是一种独特的框架，用于在器官压力与器官尺度之间的菌株与管道水平的生物调控过程中的定量联系，该方法控制肥厚性反应。然而，G＆R的微观结构动机，严格验证的计算模型仍在初期。

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