Regina Pando Gonzalez
Research Mentor(s): Andre Monteiro Da Rocha
Mentor Department: Cardiology – CVC Cardiovascular Regeneration Core
Authors: Regina Pando
Session: Session 5 (2:00pm – 2:50pm)
Presentation Type: Poster 62
Abstract
Aging significantly affects the structure and function of the heart, increasing the risk of cardiovascular diseases such as diastolic dysfunction. Among the molecular changes associated with aging are alterations in the Wnt/ß-Catenin signaling pathway, which regulates cardiac development and growth. Although this pathway is essential, its activity is low in the healthy adult heart. Overactivation of Wnt/ß-Catenin signaling has been linked to diastolic dysfunction, myocardial thickening, and fibrosis. The Wnt/ß-Catenin pathway is initiated by Wnt protein binding to frizzled receptors, inhibiting GSK3B-mediated degradation of ß-Catenin. This allows ß-Catenin to accumulate, translocate to the nucleus, and regulate target genes such as SNAI2. Pathway activation can be triggered by Wnt proteins, mechanical stress, growth factors, and hypoxia. This study investigates how aging and sex influence the expression and subcellular localization of ß-Catenin in cardiac tissue. Heart tissues from mice are grouped into four categories: old female, young female, old male, and young male. Immunohistochemistry is used to quantify ß-Catenin expression and determine its location in cardiomyocyte nuclei and cytoplasm, providing insights into pathway activity in each group. Intracellular calcium overload is a key mechanism underlying diastolic dysfunction. Changes in ß-Catenin expression have been associated with altered calcium handling, including impaired calcium transients. By analyzing the impact of aging and sex on ß-Catenin, this study aims to elucidate the mechanisms by which Wnt/ß-Catenin activation contributes to calcium dysregulation and diastolic dysfunction. Improved understanding of this relationship could pave the way for more effective treatments for age-related cardiac conditions.
