Abstract
Fibroblast activation is a hallmark feature of pathological remodeling of the heart and represents an attractive target for therapeutic intervention. Pharmacological inhibition of chromatin remodeling enzymes reduces cardiac fibrosis, but the underlying transcriptional regulatory mechanisms remain poorly understood. Using single-cell genomics to profile alterations in the transcriptional and chromatin landscape during stress-induced cardiac remodeling, Alexanian et al. discovered a critical role for Mesenchyme Homeobox 1 in the regulation of myofibroblast activation and cardiac fibrosis. We briefly review these important findings and comment on the significance of their work.
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