Abstract
How chromatin accessibility and structure endow highly specialized cells with their unique phenotypes is an area of intense investigation. In the mammalian heart, an exclusive subset of cardiac cells comprise the conduction system. Many molecular components of this system are well studied and genetic variation in some of the components induces abnormal cardiac conduction. However, genetic risk for cardiac arrhythmias in human populations also occurs in noncoding regions. A study by Bhattacharyya, Kollipara, et al. in this issue of the JCI examines how chromatin accessibility and structure may explain the mechanisms by which noncoding variants increase susceptibility to cardiac arrhythmias. We discuss the implications of these findings for cell type-specific gene regulation and highlight potential therapeutic strategies to engineer locus-specific epigenomic remodeling in vivo.
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