Key result
NBCe1 overexpression exacerbated cardiac remodeling, increased mortality, and enlarged infarct size after myocardial infarction in mice by increasing intracellular calcium overload.
Why the study?
The role of the cardiac isoform of the electrogenic sodium-bicarbonate ion cotransporter (NBCe1) in cardiac remodeling was not fully understood.
Does NBCe1 overexpression exacerbate cardiac remodeling and calcium overload in mice with myocardial infarction?
Population
NBCe1 transgenic mice with MI and NBCe1 overexpressing adult mouse ventricular myocytes
Comparison
NBCe1 overexpression vs wild-type controls
Design
Preclinical animal and cellular experimental study
Follow-up
6 weeks after MI
Authors
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NBCe1 overexpression worsens post-MI outcomes in mice; leaves open whether inhibition improves remodeling or survival in translational models.
Does NBCe1 overexpression exacerbate cardiac remodeling and calcium overload in mice with myocardial infarction?
NBCe1 overexpression exacerbates post-MI cardiac remodeling via intracellular calcium overload, suggesting NBCe1 as a potential therapeutic target.
Chen et al. (2019) studied Myocardial infarction and cardiac remodeling. NBCe1 overexpression vs. Wild-type (WT) mice and WT AMVMs was evaluated on Cardiac remodeling, mortality, infarct size, and calcium kinetics. NBCe1 overexpression exacerbated cardiac remodeling, increased mortality, and enlarged infarct size after myocardial infarction in mice by increasing intracellular calcium overload.
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