Key result
Inhibition of PI 3-kinase or down-regulation of the p110beta isoform decreased angiotensin II-induced ROS formation, while p110alpha down-regulation decreased alpha-adrenoceptor-mediated hypertrophy.
Population
Freshly isolated adult cardiomyocytes
Comparison
Inhibition of PI 3-kinase by Ly294002 or… vs Sense oligonucleotides or uninhibited state
Design
Preclinical
Authors
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Isoform-selective PI3K inhibition may differentiate ROS from hypertrophy pathways in cardiomyocytes; leaves open human translation.
The study demonstrates that different PI 3-kinase isoforms mediate distinct pathways in cardiomyocytes, with p110beta involved in Ang II-induced ROS formation and p110alpha in alpha-adrenoceptor-mediated hypertrophy.
Wenzel et al. (2006) studied this question. PI 3-kinase inhibitors and antisense oligonucleotides was evaluated on Formation of ROS, p38 MAPK phosphorylation, TGFbeta expression, and hypertrophic growth. Inhibition of PI 3-kinase or down-regulation of the p110beta isoform decreased angiotensin II-induced ROS formation, while p110alpha down-regulation decreased alpha-adrenoceptor-mediated hypertrophy.
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