【摘 要】
:
家族性心肌肥大症是一种由基因突变引起的,涉及离子通道,细胞代谢,肌丝收缩,心肌组织肥大异常等多层次,多因素相互作用的遗传性疾病。本研究在已有实验数据的基础上,构建了一个多层次的定量模型,能够系统全面地反映心肌肥大发生过程中所涉及的基因突变,离子浓度变化,代谢途径变化,肌小节收缩力改变以及最终导致心脏收缩与舒张功能异常的整个过程。该模型整合了心脏建模领域的各种理论,如反映分子层次心肌离子浓度变化的L
【机 构】
:
华中科技大学光电国家实验室Britton Chance生物医学光子学研究中心,湖北省武汉市430074
论文部分内容阅读
家族性心肌肥大症是一种由基因突变引起的,涉及离子通道,细胞代谢,肌丝收缩,心肌组织肥大异常等多层次,多因素相互作用的遗传性疾病。本研究在已有实验数据的基础上,构建了一个多层次的定量模型,能够系统全面地反映心肌肥大发生过程中所涉及的基因突变,离子浓度变化,代谢途径变化,肌小节收缩力改变以及最终导致心脏收缩与舒张功能异常的整个过程。该模型整合了心脏建模领域的各种理论,如反映分子层次心肌离子浓度变化的Luo-Rudy模型,反映亚细胞层次肌丝收缩的ODE模型,并构建了心肌细胞—心脏组织能量代谢网络,最后基于数字人心脏结构数据集,采用有限元方法对构建的心脏左心室收缩舒张过程进行了模拟分析。
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