Reduced PI3K(p110α) induces atrial myopathy, and PI3K-related lipids are dysregulated in athletes with atrial fibrillation.

ABSTRACT:

Background

Elucidating mechanisms underlying atrial myopathy, which predisposes individuals to atrial fibrillation (AF), will be critical for preventing/treating AF. In a serendipitous discovery, we identified atrial enlargement, fibrosis, and thrombi in mice with reduced phosphoinositide 3-kinase (PI3K) in cardiomyocytes. PI3K(p110α) is elevated in the heart with exercise and is critical for exercise-induced ventricular enlargement and protection, but the role in the atria was unknown. Physical inactivity and extreme endurance exercise can increase AF risk. Therefore, our objective was to investigate whether too little and/or too much PI3K alone induces cardiac pathology.

Methods

New cardiomyocyte-specific transgenic mice with increased or decreased PI3K(p110α) activity wer

SUBMITTER: Bass-Stringer S 

PROVIDER: S-EPMC11978378 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature