Key result
Phospholamban gene ablation in a mouse model of heart failure enhanced cardiomyocyte calcium transients but did not improve survival, cardiac function, or remodeling.
Why the study?
Does ablation of phospholamban expression improve cardiac function, limit remodeling, and improve survival in the TNF1.6 mouse model of heart failure?
Does ablation of phospholamban expression improve cardiac function, limit remodeling, and improve survival in the TNF1.6 mouse model of heart failure?
Enhancement of intrinsic cardiomyocyte calcium cycling via phospholamban ablation is insufficient to overcome the pathophysiologic processes of heart failure in a TNF-alpha overexpression mouse model.
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Phospholamban ablation fails to improve outcomes in this TNF-driven HF model; leaves open whether calcium cycling enhancement alone alters progression in other models.
Andrzej M. Janczewski (2004) studied Heart failure. Phospholamban gene ablation vs. TNF1.6 mice was evaluated on Survival, cardiac function, and cardiac remodeling. Phospholamban gene ablation in a mouse model of heart failure enhanced cardiomyocyte calcium transients but did not improve survival, cardiac function, or remodeling.
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