Curr Hypertens Rep
November 2024
Purpose Of The Review: The role of leptin in regulating cardiac function is still controversial with conflicting results in clinical and preclinical studies. However, most previous studies have not considered leptin's powerful cardiac effects that are mediated via activation of central nervous system (CNS) leptin receptors (LepRs) which, in turn, elicit major improvements in cardiac metabolism. In this review, we focus mainly on the role of leptin in regulating cardiac function via its CNS LepRs and downstream signaling pathways, such as the brain melanocortin system.
View Article and Find Full Text PDFBackground: Left atrial (LA) remodeling plays a significant role in the progression of atrial fibrillation (AF). Although LA wall thickness (LAWT) has emerged as an indicator of structural remodeling, its impact on AF outcomes remains unclear. We aimed to determine the association between LAWT and AF recurrence after pulmonary vein isolation (PVI), as well as to evaluate the relationship between LAWT and LA fibrosis.
View Article and Find Full Text PDFTraining in team sports such as soccer requires advanced technical and tactical skills for effective decision-making, particularly when executing a shot. This study validates an innovative instrument, a training platform (TP), designed to measure and enhance decision-making in dual-task scenarios. The TP aims to improve visual-motor reactions in multitask environments that simulate real game conditions.
View Article and Find Full Text PDFBackground: Sesn2 (Sestrin2) is a stress-induced protein that provides protective effects during myocardial ischemia and reperfusion (I/R) injury, while endoplasmic reticulum (ER) stress may be a pivotal mediator of I/R injury. The goal of this study was to determine whether Sesn2-mTOR (mammalian target of rapamycin) signaling regulates ER stress during myocardial I/R.
Methods And Results: In vivo cardiac I/R was induced by ligation and subsequent release of the left anterior descending coronary artery in wild-type (WT) and cardiac-specific Sesn2 knockout (Sesn2) mice.