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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: Smad3 in dbdb]

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE241176 | GEO | 2024/08/18

REPOSITORIES: GEO

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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]

Project description: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.

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