GEO series
YAP dysregulation triggers hypertrophy by CCN2 secretion and TGFβ uptake in human pluripotent stem cell-derived cardiomyocytes
GSE261296
Homo sapiens
Expression profiling by high throughput sequencing
12 samples
2025/01/01
GPL24676
Summary
Our research has demonstrated the following: (1) Confirmed that MYH7 mutations D239N, H251N, G256E lead to hypercontractility in hiPSC-derived cardiomyocytes (hiPSC-CMs); (2) Increase in YAP’s nuclear localization in both hiPSC-CMs and patient tissue with MYH7 HCM mutations; (3) A correlation between YAP's nuclear localization and enhanced force generation; (4) Nuclear deformation as a mechanism enabling YAP's nuclear entry and activation; (5) Transcriptomic changes resulting from positive and negative modifications in force generation; and (6) A distinctive paracrine hypertrophic signal reliant on cardiomyocyte-cardiac fibroblast crosstalk. Our unique insights to the intricacies of hypertrophic cardiomyopathy phenotypes hold the potential to provide mechanistic clarity, informing potential therapeutic strategies.
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