Key result
Non-myocyte connexins drive post-MI arrhythmias, adverse ventricular remodeling, and atherosclerosis development.
Targeting connexins in non-myocytes represents a potential novel therapeutic avenue for cardiovascular diseases including arrhythmias, post-MI remodeling, and atherosclerosis.
May support connexin targeting in non-myocytes as a therapeutic strategy for post-MI arrhythmias and atherosclerosis; hypothesis-generating and requires prospective validation before clinical adoption.
The heart is a complex organ composed of multiple cell types, including cardiomyocytes and different non-myocyte populations, all working closely together to determine the hearts properties and maintain normal cardiac function. Connexins are abundantly expressed proteins that form plasma membrane hemichannels and gap junctions between cells. Gap junctions are intracellular channels that allow for communication between cells, and in the heart they play a crucial role in cardiac conduction by coupling adjacent cardiomyocytes. Connexins are expressed in both cardiomyocytes and non-myocytes, including cardiac fibroblasts, endothelial cells, and macrophages. Non-myocytes are the largest population of cells in the heart, and therefore it is important to consider what roles connexins, hemichannels, and gap junctions play in these cell types. The aim of this review is to provide insight into connexin-based signalling in non-myocytes during health and disease, and highlight how targeting these proteins could lead to the development of novel therapies. We conclude that connexins in non-myocytes contribute to arrhythmias and adverse ventricular remodelling following myocardial infarction, and are associated with the initiation and development of atherosclerosis. Therefore, therapeutic interventions targeting these connexins represent an exciting new research avenue with great potential.
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Johnson et al. (2018) conducted a review in Cardiovascular disease. Connexin-based signalling in non-myocytes was evaluated. Connexins in non-myocytes contribute to arrhythmias and adverse ventricular remodelling following myocardial infarction, and are associated with the initiation and development of atherosclerosis.
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