Prime editing corrects the dilated cardiomyopathy causing RBM20-P633L-mutation in human cardiomyocytes

Roman et al. (2025) demonstrate prime editing efficacy in human iPSC-derived cardiomyocytes — post-mitotic cells with relevance as an OHC analogue. A PE4 strategy targeting the RBM20-P633L dilated cardiomyopathy mutation achieved approximately 35% editing efficiency in terminally differentiated cardiomyocytes, with downstream functional rescue: restored RBM20 protein localization and normalized cardiac splicing patterns for titin and calcium signaling genes. This is the first reported PE phenotypic rescue in a human post-mitotic disease model.

Author note: This paper was cited in the h07 sweep notes as “Chemla 2025 PMID 41210585.” The name “Chemla” does not appear in the author list. The actual first author is Alexandra Roman (Roman et al. 2025). This is a new author-phantom introduced in the sweep; corrected here.

Key finding

~35% prime editing efficiency in human iPSC-derived cardiomyocytes with phenotypic rescue confirms PE is mechanistically compatible with post-mitotic human cells beyond neurons. The functional rescue (splicing normalization) is the critical result — not just editing frequency.

Numbers that matter

ParameterValueUnitsSourceConditions
PE4 editing efficiency in cardiomyocytes~35% (average)AbstractHuman iPSC-derived CMs, RBM20-P633L disease model
Cell typeiPSC-derived cardiomyocytesPost-mitotic; differentiated from patient-derived iPSCs
Phenotypic rescueYesAbstractRBM20 protein localization restored; titin splicing normalized

Limitations

  • Ex vivo cell model, not in vivo delivery; AAV transduction efficiency in vivo CMs is lower than lentiviral/plasmid ex vivo.
  • iPSC-derived CMs are less mature than adult CMs; fetal-like transcriptome may affect PE machinery expression.
  • No efficiency breakdown by PE variant optimization steps; “~35%” is the reported average.
  • No OHC data; cardiomyocyte → OHC extrapolation assumes similar post-mitotic PE compatibility.

Connections