November 18, 2003CirculationOpen Access

Common Genomic Response in Different Mouse Models of β-Adrenergic–Induced Cardiomyopathy

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Population

Mice overexpressing Gsalpha, beta1AR, beta2AR, or protein kinase A

Design

Preclinical

Authors

VGVinciane GaussinRutgers New Jersey Medical School JTJames TomlinsonSheffield Teaching Hospitals NHS Foundation Trust CDChristophe DepréAmgen (United States)

Discussion

Member takes

Implication

UCP2/FHL1 merit investigation as cardiomyopathy mediators; animal data leave open human translation and therapeutic relevance.

Structured PICO

Population

Mice overexpressing Gsalpha, beta1AR, beta2AR, or protein kinase A (models of beta-adrenergic-induced cardiomyopathy)

Intervention

Beta-adrenergic receptor (AR) blockade treatment

Outcome

Differential gene expression (specifically UCP2 and FHL1) and development/reversal of cardiomyopathysurrogate

UCP2 and FHL1 are identified as key genes upregulated in beta-adrenergic-induced cardiomyopathy, and their expression is suppressed by beta-blocker therapy, providing mechanistic insight into its benefits in heart failure.

Cite This Study

Gaussin et al. (2003) studied this question.

synapsesocial.com/papers/6a70d98ffebe604dd7099f64 https://doi.org/10.1161/01.cir.0000101922.18151.7b

Topics

Cardiomyopathy Heart failure HFrEF treatment Cardiac amyloidosis

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Common Genomic Response in Different Mouse Models of β-Adrenergic–Induced Cardiomyopathy

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

Common Genomic Response in Different Mouse Models of β-Adrenergic–Induced Cardiomyopathy

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Topics

Also Consider