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Effect of cardiac SRPK3 overexpression in adult mice

GSE260494 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2024/03/05 Platform GPL24247
Summary
Pathological cardiac hypertrophy is unequivocally identified as an ominous escalation of hemodynamically stressful overload, ultimately heighten risk of sudden death as heart failure (HF) ensues. Here, we explored how dysregulated mitochondrial RNA (mtRNA) metabolism remodels mitochondrial bioenergetics and controls hypertrophic-phenotype cardiopathy in mice and humans. Utilizing targeted genetic approaches and in vivo functional imaging, we describe a potent cardiac pro-hypertrophic role for serine arginine protein kinase 3 (SRPK3), which is highly induced in myocardium upon hypertrophic stimuli. Adult extended expression of SRPK3 in cardiomyocytes (CMs) leads to spontaneously concentric hypertrophy and eventuates sudden cardiac death in mice.
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Direct links to NCBI, no account and no request form: the whole study as GSE260494_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1081882 and SRA study SRP492383. Searching any of these in the dataset finder brings you back here.

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