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首页> 外文期刊>Progress in Cardiovascular Diseases >Matrix, cytoskeleton, or myofilaments: which one to blame for diastolic left ventricular dysfunction?
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Matrix, cytoskeleton, or myofilaments: which one to blame for diastolic left ventricular dysfunction?

机译：基质，细胞骨架或肌丝：舒张性左心室功能不全应归咎于哪一个？

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During cardiac filling, the relative contribution of distension of interstitial collagen, of distension of cytoskeletal proteins, and of low-grade diastolic cross-bridge cycling in the generation of diastolic left ventricular (LV) pressure remains unclear. In failing myocardium, interstitial collagen deposition and cross-linking are augmented. This increase in collagen deposition is accompanied by expression of a stiffer isoform of titin in the cardiomyocytes. Higher diastolic stiffness of failing myocardium is therefore not necessarily related to increased interstitial collagen content. Moreover, phosporylation of titin by protein kinase A and G, and inhibition of titin-actin interaction by cytosolic calcium allow for dynamic modulation of its diastolic tension generation and could account for acute shifts of myocardial distensibility. Acute shifts of myocardial distensibility, as occur in hypertrophy or in demand ischemia, have usually been attributed to a diastolic resurgence of cross-bridge interaction. In hypertrophied and failing myocardium, the recent demonstrations of diastolic calcium release from the ryanodine receptor, of deficient diastolic calcium removal from the cytosol, and of enhanced myofilamentary calcium sensitivity support residual diastolic cross-bridge interaction. In demand ischemia, the role of calcium overload in the reduction of diastolic LV distensibility is less clear because of correction of the reduced diastolic LV distensibility by quick stretches but not by a calcium desensitizer. Simultaneous imposition in animal models of multiple molecular changes involving interstitial, cytoskeletal, and myofilamentary proteins could elucidate their relative importance for myocardial stiffness and lead to selective correction of diastolic LV dysfunction as a novel mode of heart-failure therapy.
机译：在心脏充盈过程中，在舒张期左心室（LV）压力的产生中，间质胶原蛋白的扩张，细胞骨架蛋白的扩张和低度舒张剂跨桥循环的相对贡献尚不清楚。在衰竭的心肌中，间质胶原沉积和交联增加。胶原蛋白沉积的这种增加伴随着心肌细胞中更坚硬的替丁异构体表达。因此，衰竭心肌的更高的舒张刚度不一定与间质胶原含量的增加有关。此外，蛋白激酶A和G磷酸化肌动蛋白，以及胞质钙抑制肌动蛋白与肌动蛋白的相互作用，可以动态调节其舒张张力的产生，并可以解释心肌扩张性的急剧变化。心肌肥大的急性变化，如在肥大或按需缺血中，通常归因于跨桥相互作用的舒张性恢复。在肥厚和衰竭的心肌中，最近的证据表明，舒张剂钙从ryanodine受体中释放出来，舒张剂钙从细胞溶质中的去除不足，以及增强的肌丝钙敏感性，都支持残留的舒张剂跨桥相互作用。在需求缺血中，钙超载在舒张压左室扩张性降低中的作用尚不清楚，因为通过快速拉伸而不是通过钙脱敏剂来纠正舒张压左室扩张性降低。在动物模型中同时施加多种涉及间质，细胞骨架和肌丝蛋白的分子变化，可以阐明它们对心肌僵硬的相对重要性，并导致舒张性LV功能障碍的选择性矫正，这是一种新型的心衰治疗方式。

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