Epigenetic reprogramming to prevent genetic cardiomyopathy

Jamie R. Johnston, Daniel F. Selgrade, Elizabeth M. McNally*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

Mutations in the gene that codes for lamin A/C (LMNA) are a common cause of adult-onset cardiomyopathy and heart failure. In this issue of the JCI, Guénantin and Jebeniani et al. identify impaired cardiomyocyte development and maturation as a prenatal feature in a model of laminopathy. Cardiomyocytes carrying the Lmna point mutation H222P misexpressed genes involved in the epithelial-mesenchymal transition and showed decreased methylation at the fourth lysine of histone H3 (H3K4). Notably, inhibiting lysine-specific demethylase 1 in the LMNA H222P mouse model treated this congenital form of cardiomyopathy and improved survival in utero. These data highlight early epigenomic modifications in lamin A/C-mediated pathology and indicate a unique therapeutic strategy for cardiomyopathy.

Original languageEnglish (US)
Article numbere143684
JournalJournal of Clinical Investigation
Volume131
Issue number1
DOIs
StatePublished - Jan 4 2021

ASJC Scopus subject areas

  • Medicine(all)

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