Multiscale biophysical models of cardiomyopathies reveal complexities challenging existing dogmas.
Multiscale biophysical models of cardiomyopathies reveal complexities challenging existing dogmas.
复制标题
心肌病的多尺度生物物理模型揭示了挑战现有教条的复杂性。
DOI：
10.1016/j.bpj.2023.11.014
复制
发表时间：
2023
影响因子：
3.4
通讯作者：
Greenberg,MichaelJ
中科院分区：
文献类型：
--
作者：
Scott,Brent;Greenberg,MichaelJ
包括肌球蛋白在内的肌节蛋白突变会导致多种心肌疾病。一个突出的假说是，肌球蛋白突变导致运动的过度收缩会导致肥厚性心肌病，而那些引起收缩能力低下的突变会导致扩张型心肌病；然而，最近使用多尺度计算和实验模型进行的生物物理研究揭示了这一假说没有捕捉到的复杂性。我们总结了最近在生物物理杂志上发表的挑战这一教条的文章，并强调了对这些复杂疾病进行多尺度建模的必要性。
Mutations in sarcomeric proteins, including myosin, cause a variety of cardiomyopathies. A prominent hypothesis has been that myosin mutations causing hypercontractility of the motor lead to hypertrophic cardiomyopathy, while those causing hypocontractility lead to dilated cardiomyopathy; however, recent biophysical studies using multiscale computational and experimental models have revealed complexities not captured by this hypothesis. We summarize recent publications inBiophysical Journalchallenging this dogma and highlighting the need for multiscale modeling of these complex diseases.