期刊
PHYSIOLOGICAL REVIEWS
卷 103, 期 3, 页码 2271-2319出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physrev.00021.2022
关键词
arrhythmia; cardiac physiology; cell adhesion; gap junction; intercalated disc
类别
The intercalated disc (ID) is a specialized structure that connects cardiomyocytes via mechanical and electrical junctions. Recent studies have revealed the complex nanostructure and molecular composition of the ID, highlighting the fact that it is not just a simple cell-to-cell coupling junction but rather an interacting molecular complex. Understanding the physiological implications of the ID architecture and the local intermolecular interactions is crucial for understanding normal cardiac conduction and the pathophysiology of arrhythmias.
The intercalated disc (ID) is a highly specialized structure that connects cardiomyocytes via mechanical and electrical junctions. Although described in some detail by light microscopy in the 19th century, it was in 1966 that electron microscopy images showed that the ID represented apposing cell borders and provided detailed insight into the complex ID nanostructure. Since then, much has been learned about the ID and its molecular composition, and it has become evident that a large number of proteins, not all of them involved in direct cell -to-cell coupling via mechanical or gap junctions, reside at the ID. Furthermore, an increasing number of func-tional interactions between ID components are emerging, leading to the concept that the ID is not the sum of isolated molecular silos but an interacting molecular complex, an organelle where components work in concert to bring about electrical and mechanical synchrony. The aim of the present review is to give a short historical account of the ID's discovery and an updated overview of its composition and organization, followed by a dis-cussion of the physiological implications of the ID architecture and the local intermolecular interactions. The lat-ter will focus on both the importance of normal conduction of cardiac action potentials as well as the impact on the pathophysiology of arrhythmias.
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