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心脏缝隙连接细胞-细胞偶联的重构。

Remodeling of Cardiac Gap Junctional Cell-Cell Coupling.

机构信息

Institute for Pharmacology, University Leipzig, Härtelstr. 16, 04103 Leipzig, Germany.

Fachdienst Gesundheit, Lindenaustr. 31, 04600 Altenburg, Germany.

出版信息

Cells. 2021 Sep 14;10(9):2422. doi: 10.3390/cells10092422.

Abstract

The heart works as a functional syncytium, which is realized via cell-cell coupling maintained by gap junction channels. These channels connect two adjacent cells, so that action potentials can be transferred. Each cell contributes a hexameric hemichannel (=connexon), formed by protein subuntis named connexins. These hemichannels dock to each other and form the gap junction channel. This channel works as a low ohmic resistor also allowing the passage of small molecules up to 1000 Dalton. Connexins are a protein family comprising of 21 isoforms in humans. In the heart, the main isoforms are Cx43 (the 43 kDa connexin; ubiquitous), Cx40 (mostly in atrium and specific conduction system), and Cx45 (in early developmental states, in the conduction system, and between fibroblasts and cardiomyocytes). These gap junction channels are mainly located at the polar region of the cardiomyocytes and thus contribute to the anisotropic pattern of cardiac electrical conductivity. While in the beginning the cell-cell coupling was considered to be static, similar to an anatomically defined structure, we have learned in the past decades that gap junctions are also subject to cardiac remodeling processes in cardiac disease such as atrial fibrillation, myocardial infarction, or cardiomyopathy. The underlying remodeling processes include the modulation of connexin expression by e.g., angiotensin, endothelin, or catecholamines, as well as the modulation of the localization of the gap junctions e.g., by the direction and strength of local mechanical forces. A reduction in connexin expression can result in a reduced conduction velocity. The alteration of gap junction localization has been shown to result in altered pathways of conduction and altered anisotropy. In particular, it can produce or contribute to non-uniformity of anisotropy, and thereby can pre-form an arrhythmogenic substrate. Interestingly, these remodeling processes seem to be susceptible to certain pharmacological treatment.

摘要

心脏作为一个功能整体发挥作用,这是通过缝隙连接通道维持的细胞-细胞偶联实现的。这些通道连接两个相邻的细胞,以便可以传递动作电位。每个细胞贡献一个由连接蛋白亚基组成的六聚体半通道(=连接子)。这些半通道彼此对接,形成缝隙连接通道。该通道作为一个低欧姆电阻器起作用,也允许小分子(高达 1000 道尔顿)通过。连接蛋白是一个由 21 个人类同工型组成的蛋白家族。在心脏中,主要的同工型是 Cx43(43kDa 连接蛋白;普遍存在)、Cx40(主要存在于心房和特定的传导系统)和 Cx45(在早期发育阶段、传导系统中和成纤维细胞与心肌细胞之间)。这些缝隙连接通道主要位于心肌细胞的极区,因此有助于心脏电导率的各向异性模式。虽然最初细胞-细胞偶联被认为是静态的,类似于解剖学定义的结构,但在过去几十年中,我们了解到缝隙连接也受心脏疾病(如心房颤动、心肌梗死或心肌病)中的心脏重塑过程的影响。潜在的重塑过程包括连接蛋白表达的调制,例如血管紧张素、内皮素或儿茶酚胺,以及缝隙连接定位的调制,例如通过局部机械力的方向和强度。连接蛋白表达的减少可导致传导速度降低。缝隙连接定位的改变已被证明会导致传导途径的改变和各向异性的改变。特别是,它可以产生或有助于各向异性的非均匀性,并因此可以预先形成心律失常的基质。有趣的是,这些重塑过程似乎容易受到某些药物治疗的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d9cd/8465208/bb10b50aa48c/cells-10-02422-g001.jpg

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