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

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.

Molecular Imaging of Diffuse Cardiac Fibrosis with a Radiotracer That Targets Proteolyzed Collagen IV.

Purpose To develop an approach for in vivo detection of interstitial cardiac fibrosis using PET with a peptide tracer targeting proteolyzed collagen IV (T-peptide). Materials and Methods T-peptide was conjugated to the copper chelator MeCOSar (chemical name, 5-(8-methyl-3,6,10,13,16,19-hexaaza-bicyclo[6.6.

PI3K signalling at the intersection of cardio-oncology networks: cardiac safety in the era of AI.

Class I phosphoinositide 3-kinases (PI3Ks) are a family of lipid kinases. They are super elevated in many human cancer types and exert their main cellular functions by activating Akt to trigger an array of distinct responses, affecting metabolism and cell polarity. The signal equally plays important roles in cardiovascular pathophysiology.

PI3K(p110α) as a determinant and gene therapy for atrial enlargement in atrial fibrillation.

Atrial fibrillation (AF) is an irregular heart rhythm, characterised by chaotic atrial activation, which is promoted by remodelling. Once initiated, AF can also propagate the progression of itself in the so-called ''AF begets AF''. Several lines of investigation have shown that signalling molecules, including reactive oxygen species, angiotensin II, and phosphoinositide 3-kinases (PI3Ks), in presence or absence of cardiovascular disease risk factors, stabilise and promote AF maintenance.

Assessment of the epi-pericardial fibrotic substrate by collagen-targeted probes.

The identification of the fibrotic arrhythmogenic substrate as a means of improving the diagnosis and prediction of atrial fibrillation has been a focus of research for many years. The relationship between the degree of atrial fibrosis as a major component of atrial cardiomyopathy and the recurrence of arrhythmia after AF ablation can correlate. While the focus in identification and characterisation of this substrate has been centred on the atrial wall and the evaluation of atrial scar and extracellular matrix (ECM) expansion by late gadolinium-enhancement (LGE) on cardiac magnetic resonance imaging (CMRI), LGE cannot visualise diffuse fibrosis and diffuse extravasation of gadolinium.