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Fibroblast-specific TGF-b signaling mediates dysfunction, fibrosis and hypertrophy in a mouse model of obesity-associated type 2 diabetes [RNA-seq: TSP4 OE]

GSE241178 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2024/08/18 Platform GPL24247
Summary
Our study provides the first direct evidence supporting a fibroblast-mediated mechanism of dysfunction and adverse remodeling in the diabetic heart, highlighting the importance of interstitial cells in the pathogenesis of diabetic cardiomyopathy. Diabetes-associated activation of the TGF-b/Smad3 cascade may promote dysfunction not only by accentuating ECM deposition and crosslinking, but also by modulating cardiomyocyte phenotype and function. Thus, the TGF-b system may be a promising therapeutic target in patients with diabetes-associated heart failure.
Published in
Fibroblast-specific TGF-β signaling mediates cardiac dysfunction, fibrosis, and hypertrophy in obese diabetic mice
Tuleta I, Hanna A, Humeres C et al. · Cardiovascular research 2024 · PMID 39373248 · doi:10.1093/cvr/cvae210
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Also filed as BioProject PRJNA1006688 and SRA study SRP455799. Searching any of these in the dataset finder brings you back here.

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