Eita Shinkawa
Research Mentor(s): Morgan Salmon
Mentor Department: Cardiac Surgery
Authors: Eita Shinkawa, Jessee Khan, Gorav Ailawadi, Morgan Salmon
Session: Session 5 (2:00pm – 2:50pm)
Presentation Type: Poster 69
Abstract
Abdominal Aortic Aneurysms (AAA) remain a leading cause of mortality in patients over the age of 65. The prevalence of AAA, especially in men, has dramatically increased in recent years, with 10% of men above the age of 85 showing signs of AAA. Symptoms, though uncommon, develop only when the aneurysm has reached a perilous size (100-150% dilation) and is at highest risk for dissection or rupture. Risk factors for AAAs include age, sex, smoking history, hypertension and increased atherosclerosis. Despite their prevalence, the mechanisms driving AAA progression, particularly in relation to aging, have not been extensively studied. During the aging process, the tissues of the aorta exhibit increased levels of proteins such as p21, p16, and p53. These proteins are associated with cellular senescence, a state characterized by the prevention of cell division and the secretion of pro-inflammatory factors collectively known as the Senescence-Associated Secretory Phenotype (SASP). Senescence plays a dual role in aging and disease, yet its precise relationship with AAAs remains unclear. This project aims to investigate the role of senescence in AAA progression using human aneurysm tissue versus controls. By analyzing the impact of senescence-associated proteins and their pathways, the study seeks to uncover how age-related cellular changes could contribute to AAA vulnerability. The goal for the current semester was to examine levels of p21, p53, Rb, p16 and lipofuscin staining in human aneurysm tissue versus controls to determine if levels of these proteins are elevated in aged aneurysms in humans. Future studies will seek to understand the effect of senescence treatment with ABT-263 could affect factors such as the prevalence of T-cells, proliferation, apoptosis, and other damaging characteristics of AAA. Through this research, the lab is exploring senescence-blocking (senolytic) therapies, including pharmacological agents, to assess their potential in preventing AAA development in older patients. This research could pave the way for novel therapeutic approaches to mitigate AAA risk and improve patient outcomes.
