Why the study?
The physiologic relevance of electrical coupling between myocytes and fibroblasts and its impact on cardiac excitability in vivo had never been demonstrated.
Fibroblasts in myocardial scar tissue can electrically couple with myocytes via gap junctional and ephaptic mechanisms, directly driving cardiac excitation and arrhythmogenesis in vivo.
May promote post-injury arrhythmias via fibroblast-myocyte coupling; hypothesis-generating in mice and requires human validation.
After heart injury, dead heart muscle is replaced by scar tissue. Fibroblasts can electrically couple with myocytes, and changes in fibroblast membrane potential can lead to myocyte excitability, which suggests that fibroblast-myocyte coupling in scar tissue may be responsible for arrhythmogenesis. However, the physiologic relevance of electrical coupling of myocytes and fibroblasts and its impact on cardiac excitability in vivo have never been demonstrated. We genetically engineered a mouse that expresses the optogenetic cationic channel ChR2 (H134R) exclusively in cardiac fibroblasts. After myocardial infarction, optical stimulation of scar tissue elicited organ-wide cardiac excitation and induced arrhythmias in these animals. Complementing computational modeling with experimental approaches, we showed that gap junctional and ephaptic coupling, in a synergistic yet functionally redundant manner, excited myocytes coupled to fibroblasts.
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Wang et al. (2023) studied this question.
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