Posters
Presenting Author Academic/Professional Position
Community Partner
Presentation Type
Poster
Discipline Track
Clinical Science
Abstract Type
Program Abstract
Abstract
Reactive oxygen species (ROS) are formed in metabolism, cellular signaling, immune response, antimicrobial defense, and detoxification. Oxidative damage through overproduction of ROS or dysregulation of ROS regulation may result in oxidative stress associated with DNA damage, protein damage, mitochondrial dysfunction, and lipid peroxidation. Additionally, the accumulation of dysfunction of cellular components may manifest as diseases that contribute to the predisposition of acute coronary syndrome (ACS). This poster meticulously explores the significance of ROS in various cardiovascular stressors, including hypertension, thrombogenesis, vascular remodeling, lipid peroxidation, cellular proliferation, atherogenesis, and vasoconstriction. These stressors collectively contribute to ACS associated with ischemia. Furthermore, autophagic function by lysosomes during cardiac arrest is compromised, which is related to ROS dysregulating lysosomal-associated membrane proteins following sudden cardiac events. Correlations have been established between ROS culprits, particularly the upregulation of NADPH oxidase, nitric oxide synthase, and the accelerated progression of atherosclerosis and ACS. Similar mechanisms of increased oxidative stress have also been associated with vasoconstriction and thrombosis. In this presentation, we will discuss the particular role of ROS in the pathogenesis of ACS, and further explore related therapies, aiming to mitigate the damaging effects of oxidative stress.
Recommended Citation
Cisneros, Fernando and Zuo, Alex, "Reactive Oxygen Species in Acute Coronary Syndrome" (2024). Research Symposium. 58.
https://scholarworks.utrgv.edu/somrs/2024/posters/58
Reactive Oxygen Species in Acute Coronary Syndrome
Reactive oxygen species (ROS) are formed in metabolism, cellular signaling, immune response, antimicrobial defense, and detoxification. Oxidative damage through overproduction of ROS or dysregulation of ROS regulation may result in oxidative stress associated with DNA damage, protein damage, mitochondrial dysfunction, and lipid peroxidation. Additionally, the accumulation of dysfunction of cellular components may manifest as diseases that contribute to the predisposition of acute coronary syndrome (ACS). This poster meticulously explores the significance of ROS in various cardiovascular stressors, including hypertension, thrombogenesis, vascular remodeling, lipid peroxidation, cellular proliferation, atherogenesis, and vasoconstriction. These stressors collectively contribute to ACS associated with ischemia. Furthermore, autophagic function by lysosomes during cardiac arrest is compromised, which is related to ROS dysregulating lysosomal-associated membrane proteins following sudden cardiac events. Correlations have been established between ROS culprits, particularly the upregulation of NADPH oxidase, nitric oxide synthase, and the accelerated progression of atherosclerosis and ACS. Similar mechanisms of increased oxidative stress have also been associated with vasoconstriction and thrombosis. In this presentation, we will discuss the particular role of ROS in the pathogenesis of ACS, and further explore related therapies, aiming to mitigate the damaging effects of oxidative stress.
