Malik Alabbas
Pronouns: He/Him
Research Mentor(s): Salim Hayek
Research Mentor School/College/Department: Internal Medicine – Cardiology / Medicine
Program:
Authors:
Session: Session 4: 1:40 pm – 2:30 pm
Poster: 58
Abstract
Cardiovascular disease (CVD) stands as the foremost cause of mortality on a global scale, with atherosclerosis emerging as a prominent subtype imposing a disproportionate burden on millions worldwide. The prevailing approach to atherosclerosis management centers on mitigating classical risk factors, such as hypertension, hyperlipidemia, obesity, and diabetes mellitus[]. However, chronic inflammation has emerged as a pivotal component contributing to residual risk, underscored by recent advancements in anti-inflammatory therapeutics showing promise in the treatment of athresclerosis[]. Soluble urokinase plasminogen activator receptor (suPAR) represents the soluble form of uPAR, a three domain receptor protein distributed across various cell membranes[]. Recent investigations have implicated suPAR as a principal regulator in the pathogenesis of atherosclerosis. A study spearheaded by Hayek et al. has amassed clinical, genetic, and experimental evidence endorsing suPAR’s role as a pathogenic agent in atherosclerosis. Notably, suPAR fosters atherosclerosis by modulating monocyte activation and functionality, thereby positing suPAR levels as intrinsically intertwined with the pathway’s activity in atherosclerosis. The present study scrutinizes the precedent of suPAR as a regulator of monocyte differentiation. Utilizing differentiated THP-1 M0 monocytes, we subjected them to suPAR treatment, conducting a series of immunoassays to probe the inflammatory profiles of the ensuing macrophages. We posit that suPAR induces proinflammatory phenotypes in macrophages, which is in line with our broader understanding of suPARs role in inflammation in the pathogenesis of atherosclerosis.
