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[细肌丝激活的协同机制对心肌收缩功能的贡献。通过数学模型进行评估]

[Contribution of cooperative mechanisms of the thin filament activation to the myocardium contractile function. Assessment by a mathematical model].

作者信息

Kantsel'son L B, Sul'man T B, Solov'eva O E, Markhasin V S

出版信息

Biofizika. 2009 Jan-Feb;54(1):53-61.

Abstract

We applied a mathematical model to compare the contributions to the myocardium mechanical activity of two a priori feasible variants of the cooperative effect of myosin cross-bridges on the calcium activation of sarcomere thin filaments. One of these variants implies that cross-bridge cooperative influence on the troponin C affinity to calcium is localized within the same functional cluster A7TmTn where the cross-bridge is attached. The second variant is based on the assumption that cross-bridges may affect the affinity of troponin C to calcium in other functional clusters A7TmTn as well (so that the nearer to the cross-bridge a cluster lies, the stronger the cross-bridge affects the affinity of CaTnC complex in this cluster). Each of these two variants and its contribution to the active mechanical performance of the heart muscle during the contraction-relaxation cycle were alternatively assessed in the model. It was found that only the second variant correctly simulates the mechanical activity of the muscle. Thus, the modeling suggests that just this variant of the cooperativity seems to be more feasible.

摘要

我们应用了一个数学模型,来比较肌球蛋白横桥对肌节细肌丝钙激活的协同效应的两种先验可行变体对心肌机械活动的贡献。其中一种变体意味着,横桥对肌钙蛋白C与钙亲和力的协同影响局限于横桥附着的同一功能簇A7TmTn内。第二种变体基于这样的假设,即横桥也可能影响其他功能簇A7TmTn中肌钙蛋白C与钙的亲和力(因此,一个簇离横桥越近,横桥对该簇中CaTnC复合物亲和力的影响就越强)。在模型中,对这两种变体中的每一种及其在收缩-舒张周期中对心肌主动机械性能的贡献进行了交替评估。结果发现,只有第二种变体正确模拟了肌肉的机械活动。因此,建模表明,正是这种协同作用变体似乎更可行。

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