July 21, 2014BMC Cardiovascular DisordersOpen Access

Resistance to cardiomyocyte hypertrophy in ae3 −/− mice, deficient in the AE3 Cl−/HCO3−exchanger

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Why the study?

Does AE3 deficiency prevent cardiomyocyte hypertrophy in response to hypertrophic stimuli in mice?

Population

AE3-deficient (ae3-/-) mice and cultured cardiomyocytes

Comparison

Genetic deficiency of AE3 and exposure to… vs Wildtype littermates and WT cultured…

Design

Preclinical

Authors

DSDaniel SowahUniversity of Alberta BBBrittany F. BrownCollege of Staten Island AQAnita QuonUniversity of Alberta

Discussion

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Implication

AE3 deficiency blunts agonist-induced hypertrophy in mouse cardiomyocytes; leaves open AE3 as therapeutic target pending human studies.

Structured PICO

Does AE3 deficiency prevent cardiomyocyte hypertrophy in response to hypertrophic stimuli in mice?

Population

AE3-deficient (ae3-/-) mice and cultured cardiomyocytes

Intervention

Genetic deficiency of AE3 (ae3-/-) and exposure to hypertrophic stimuli

Comparator

Wildtype (WT) littermates and WT cultured cardiomyocytes

Outcome

Development of cardiomyocyte hypertrophy (assessed by echocardiography, cardiac growth, fetal gene program reactivation, and pH regulation capacity)surrogate

AE3-mediated Cl-/HCO3- exchange is crucial for the development of cardiomyocyte hypertrophy, suggesting AE3 antagonism as a potential therapeutic target for heart failure.

Cite This Study

Sowah et al. (2014) studied this question.

synapsesocial.com/papers/6a714cc335aa2c282ce29b9b https://doi.org/10.1186/1471-2261-14-89

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Resistance to cardiomyocyte hypertrophy in ae3 −/− mice, deficient in the AE3 Cl−/HCO3−exchanger

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Resistance to cardiomyocyte hypertrophy in ae3 −/− mice, deficient in the AE3 Cl−/HCO3−exchanger

Discussion

Member takes

Implication

Structured PICO

Cite This Study

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