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Cardiac reprogramming and Gata4 overexpression reduce fibrosis and improve diastolic dysfunction in heart failure with preserved ejection fraction [RNA-seq]

GSE218733 Mus musculus Expression profiling by high throughput sequencing 9 samples Submitted 2024/12/14 Platform GPL19057
Summary
Fibrosis is important pathogenesis in heart failure with preserved ejection fraction (HFpEF). We previously reported that the overexpression of cardiac transcription factors, Mef2c/Gata4/Tbx5/Hand2 (MGTH) could directly reprogram cardiac fibroblasts (CFs) into induced CMs (iCMs) and reduce fibrosis. Here we show that in vivo cardiac reprogramming generated iCMs from resident CFs, improved cardiac function, and reversed fibrosis in HFpEF model using a novel transgenic mouse system. RNA-seq revealed that the MGTH activated the cardiac program and concomitantly suppressed fibroblast and inflammatory signatures. Thus, cardiac reprogramming improves HFpEF via myocardial regeneration and anti-fibrosis.
Published in
Cardiac Reprogramming and Gata4 Overexpression Reduce Fibrosis and Improve Diastolic Dysfunction in Heart Failure With Preserved Ejection Fraction
Yamada Y, Sadahiro T, Nakano K et al. · Circulation 2025 · PMID 39673349 · doi:10.1161/CIRCULATIONAHA.123.067504
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Also filed as BioProject PRJNA905370 and SRA study SRP409763. Searching any of these in the dataset finder brings you back here.

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