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胶原蛋白与心肌:与肥大及其消退相关的纤维结构、生物合成与降解

Collagen and the myocardium: fibrillar structure, biosynthesis and degradation in relation to hypertrophy and its regression.

作者信息

Eghbali M, Weber K T

机构信息

Cardiovascular Institute, Michael Reese Hospital, University of Chicago Pritzker School of Medicine, IL 60616.

出版信息

Mol Cell Biochem. 1990 Jul 17;96(1):1-14. doi: 10.1007/BF00228448.

Abstract

The extracellular matrix of the myocardium contains an elaborate structural matrix composed mainly of fibrillar types I and III collagen. This matrix is responsible for the support and alignment of myocytes and capillaries. Because of its alignment, location, configuration and tensile strength, relative to cardiac myocytes, the collagen matrix represents a major determinant of myocardial stiffness. Cardiac fibroblasts, not myocytes, contain the mRNA for these fibrillar collagens. In the hypertrophic remodeling of the myocardium that accompanies arterial hypertension, a progressive structural and biochemical remodeling of the matrix follows enhanced collagen gene expression. The resultant significant accumulation of collagen in the interstitium and around intramyocardial coronary arteries, or interstitial and perivascular fibrosis, represents a pathologic remodeling of the myocardium that compromises this normally efficient pump. This report reviews the structural nature, biosynthesis and degradation of collagen in the normal and hypertrophied myocardium. It suggests that interstitial heart disease, or the disproportionate growth of the extracellular matrix relative to myocyte hypertrophy, is an entity that merits greater understanding, particularly the factors regulating types I and III collagen gene expression and their degradation.

摘要

心肌的细胞外基质包含一个主要由I型和III型纤维状胶原蛋白组成的精细结构基质。该基质负责心肌细胞和毛细血管的支撑与排列。由于其排列、位置、构型和拉伸强度,相对于心肌细胞而言,胶原基质是心肌僵硬度的主要决定因素。心脏成纤维细胞而非心肌细胞含有这些纤维状胶原蛋白的信使核糖核酸。在伴随动脉高血压的心肌肥厚性重塑过程中,随着胶原基因表达增强,基质会发生渐进性的结构和生化重塑。间质和心肌内冠状动脉周围胶原的显著积聚,即间质和血管周围纤维化,代表了心肌的病理性重塑,损害了这个通常高效的泵。本报告回顾了正常和肥厚心肌中胶原蛋白的结构性质、生物合成及降解。研究表明,间质心脏病,即相对于心肌细胞肥大而言细胞外基质的过度生长,是一个值得深入了解的实体,尤其是调节I型和III型胶原基因表达及其降解的因素。

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