Key result
Genetic ablation of both p110α and p110β in mouse cardiac myocytes caused heart failure, death, and T-tubule disorganization by mislocalizing junctophilin-2.
Population
Mice with genetic ablation of both p110α and p110β in cardiac myocytes throughout development or in adulthood
Design
Preclinical
Authors
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Potential cardiotoxicity risk with dual PI3K inhibitors; hypothesis-generating in mice and leaves open human relevance.
PI3K p110α and p110β are essential for maintaining T-tubule organization and cardiac contractility, highlighting a potential cardiotoxic risk for dual PI3K inhibitors used in oncology.
Wu et al. (2011) studied Heart failure. Genetic ablation of p110α and p110β was evaluated on Heart failure, death, and T-tubule organization. Genetic ablation of both p110α and p110β in mouse cardiac myocytes caused heart failure, death, and T-tubule disorganization by mislocalizing junctophilin-2.
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