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哺乳动物心脏兴奋-收缩偶联的个体发生

Ontogeny of excitation-contraction coupling in the mammalian heart.

作者信息

Tibbits Glen F, Xu Liqun, Sedarat Franklin

机构信息

Cardiac Membrane Research Laboratory, Simon Fraser University, Burnaby, BC, V5A 1S6, Canada.

出版信息

Comp Biochem Physiol A Mol Integr Physiol. 2002 Aug;132(4):691-8. doi: 10.1016/s1095-6433(02)00128-9.

Abstract

The neonate mammalian heart is phenotypically different from the adult heart in many respects. Understanding these phenotypic differences are a fundamental component of understanding the mechanisms of congenital heart disease and its treatment. Differences in excitation-contraction (E-C) coupling of the neonatal heart from that of the adult include less reliance on intercellular sources of Ca(2+) such as that from sarcoplasmic reticulum (SR). Electron micrographs indicate that these immature cardiomyocytes lack transverse tubules and the SR is sparse. This paper focuses on the changes in the phenotype of E-C coupling during ontogeny in the mammalian heart and the molecular mechanisms underlying these changes.

摘要

新生哺乳动物的心脏在许多方面与成年心脏的表型不同。了解这些表型差异是理解先天性心脏病机制及其治疗方法的基本组成部分。新生心脏与成年心脏兴奋 - 收缩(E-C)偶联的差异包括对细胞内钙(Ca(2+))来源(如肌浆网(SR))的依赖较少。电子显微镜照片显示,这些未成熟的心肌细胞缺乏横管,且肌浆网稀疏。本文重点关注哺乳动物心脏个体发育过程中E-C偶联表型的变化以及这些变化背后的分子机制。

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