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

GSE218757 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2024/12/14 Platform GPL24247
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. scRNA-seq of non-cardiomyocytes revealed that cardiac reprogramming suppressed fibroblastic gene expression via conversion of profibrotic profile to a quiescent state. Thus, in vivo cardiac reprogramming may be a promising approach for HFpEF.
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 PRJNA905412 and SRA study SRP409793. Searching any of these in the dataset finder brings you back here.

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