RUNX1-driven endothelial-to-mesenchymal transition contributes to remodelling in LMNA cardiomyopathy.
RUNX1-driven EndoMT represents a central mechanism linking LMNA mutations to fibrotic remodelling in LMNA cardiomyopathy and supports endothelial transcriptional reprogramming and RUNX1 signalling as potential therapeutic targets in fibrotic cardiomyopathy.