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肥厚、压力超负荷心肌中的胶原蛋白。

Collagen in the hypertrophied, pressure-overloaded myocardium.

作者信息

Weber K T, Janicki J S, Pick R, Abrahams C, Shroff S G, Bashey R I, Chen R M

出版信息

Circulation. 1987 Jan;75(1 Pt 2):I40-7.

PMID:2947751
Abstract

The extracellular structural protein, collagen, is responsible for the functional integrity of the myocardium permitting reversible interdigitation and transmission of force between contracting myocytes. In the pressure-overloaded, hypertrophied myocardium, clinical and experimental evidence indicates that the proportion of collagen relative to muscle is increased. Factors that appear to influence collagen growth during the hypertrophic process include age, species, the rapidity with which the overload occurs, the nature of the lesion leading to the pressure-overload, and the severity and duration of the overload. Morphologically, the heart's collagen matrix consists of a complex weave with tendinous insertions that surrounds myocytes grouping them into myofibers, strands of collagen that connect adjoining myofibers, and collagenous struts that join myocytes to other myocytes and capillaries. In a primate preparation of perinephritis with systemic hypertension, it was observed that the tendinous elements of the weave and the strands of collagen lying between myofibers were increased in number and physical dimension. The functional consequences of a remodeling of the collagen matrix that accompanied myocardial hypertrophy remain to be elucidated. A better understanding of the dynamic behavior of the collagen matrix may offer new insights into the pathogenesis of ventricular dysfunction that accompanies the chronic pressure-overloaded state.

摘要

细胞外结构蛋白胶原蛋白负责心肌的功能完整性,使收缩的心肌细胞之间能够进行可逆的相互交错和力的传递。在压力超负荷的肥厚心肌中,临床和实验证据表明,胶原蛋白相对于肌肉的比例增加。在肥厚过程中似乎影响胶原蛋白生长的因素包括年龄、物种、超负荷发生的速度、导致压力超负荷的病变性质以及超负荷的严重程度和持续时间。从形态学上讲,心脏的胶原基质由一个复杂的编织结构组成,带有腱性附着,围绕着心肌细胞将它们分组为肌纤维束,连接相邻肌纤维束的胶原束,以及将心肌细胞与其他心肌细胞和毛细血管连接起来的胶原支柱。在一只患有系统性高血压的灵长类动物肾盂肾炎模型中,观察到编织结构的腱性成分和位于肌纤维束之间的胶原束在数量和物理尺寸上都增加了。伴随心肌肥厚的胶原基质重塑的功能后果仍有待阐明。更好地理解胶原基质的动态行为可能为伴随慢性压力超负荷状态的心室功能障碍的发病机制提供新的见解。

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