Key result
Ankrd1 deletion completely abrogated phenylephrine-induced cardiomyocyte hypertrophy and fetal gene program reactivation, but did not affect hypertrophy from transverse aortic constriction.
Why the study?
Does targeted inhibition of ANKRD1 prevent phenylephrine-induced cardiomyocyte hypertrophy in preclinical models?
Population
Neonatal rat ventricular myocytes and wild-type/Ankrd1 null mice
Comparison
Knockdown of Ankrd1 / Ankrd1 null mice subjected… vs Wild-type mice and control cells
Design
Preclinical
Authors
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May inform selective ANKRD1 targeting in adrenergic models; leaves open relevance to pressure overload and human translation.
Does targeted inhibition of ANKRD1 prevent phenylephrine-induced cardiomyocyte hypertrophy in preclinical models?
ANKRD1 is a selective regulator of phenylephrine-induced hypertrophic signaling, and its inhibition abrogates PE-induced cardiomyocyte hypertrophy but not hemodynamic overload-induced hypertrophy.
Zhong et al. (2015) studied Cardiomyocyte hypertrophy. Ankrd1 knockdown or deletion vs. Wild-type mice or control cells was evaluated on Phenylephrine-induced cardiac hypertrophy and gene expression. Ankrd1 deletion completely abrogated phenylephrine-induced cardiomyocyte hypertrophy and fetal gene program reactivation, but did not affect hypertrophy from transverse aortic constriction.
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