Presentation Type
Poster
Discipline Track
Clinical Science
Abstract Type
Program Abstract
Abstract
Background: Reactive oxygen species (ROS) have diverse functions in biomedicine, providing roles in cellular metabolism and signaling while posing a threat to cellular components through oxidative damage. This poster explores the significance of ROS in various cardiovascular diseases, specifically hypertension, atherosclerosis, and myocardial infarction, all of which are associated with acute coronary syndrome which are the conditions and symptoms caused by ischemia. We have studied over 30 most recent or related literature to the topic and determine important roles of ROS in cardiovascular disease. Correlations have linked ROS culprits, particularly upregulation of NADPH oxidase (NOX) 2 and NOX 4, with accelerated progression of atherosclerosis and acute coronary syndrome. Similar mechanisms of increased oxidative stress have also been associated with vasoconstriction and thrombosis. Furthermore, auto-phagosome function by lysosomes during cardiac arrest and return of spontaneous circulation (CA-ROSC) has proven to be impaired due to ROS dysregulating Beclin-1 and lysosomal-associated membrane protein 2 (LAMP2) following sudden cardiac events. Thus, minimizing levels of ROS can potentially prevent, reduce, and minimize myocardial injury. This understanding of ROS in biomedicine guides innovative therapies to restore redox balance and reduce the detrimental effects of oxidative stress.
Methods: We systematically reviewed over 30 recent and pertinent studies on reactive oxygen species (ROS) in cardiovascular diseases, employing diverse online databases, including PubMed, Google Scholar, and Web of Science. Our objective was to consolidate crucial findings from the most recent research, forming a comprehensive framework that encompasses the current understanding of the involvement of ROS in cardiac disorders. It is noteworthy that all statistical analyses cited in the literature were conducted by the respective authors of the individual studies.
Results: Reactive oxygen species (ROS) play a crucial role in cell signaling, immune response, and gene expression. However, an excess of ROS can result in oxidative stress and cellular dysfunction. This stress disrupts intracellular processes such as programmed cell death, downstream signaling, and cellular proliferation. Consequently, tissues experiencing oxidative stress undergo alterations in their regular functioning, leading to the development of diseases. In the pathogenesis of coronary heart disease, ROS are significant contributors, influencing hypertension, atherosclerosis, and thrombosis, all of which contribute to the likelihood of acute coronary syndrome. ROS production modifies LDL, causing the formation of atherosclerotic plaques. Increased ROS production in vascular smooth muscle cells and impaired endothelial function promote the development of atherosclerosis. Additionally, elevated glucose levels facilitate the formation of platelet-monocyte aggregates in diabetic patients, thereby increasing the risk of coronary artery disease.
Conclusions: This study emphasizes the crucial involvement of reactive oxygen species (ROS) in diverse cellular mechanisms, encompassing cell signaling, immune response, and gene expression. Nevertheless, an overabundance of ROS can trigger oxidative stress, perturbing vital intracellular functions and paving the way for cardiac diseases, ultimately culminating in acute coronary syndrome. Promising therapeutic approaches, such as polyphenols and ROS scavengers, present potential avenues for alleviating oxidative stress by modulating these physiological mechanisms.
Academic/Professional Position
Faculty
Mentor/PI Department
Medical Education
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
Included in
Reactive Oxygen Species in Acute Coronary Syndrome
Background: Reactive oxygen species (ROS) have diverse functions in biomedicine, providing roles in cellular metabolism and signaling while posing a threat to cellular components through oxidative damage. This poster explores the significance of ROS in various cardiovascular diseases, specifically hypertension, atherosclerosis, and myocardial infarction, all of which are associated with acute coronary syndrome which are the conditions and symptoms caused by ischemia. We have studied over 30 most recent or related literature to the topic and determine important roles of ROS in cardiovascular disease. Correlations have linked ROS culprits, particularly upregulation of NADPH oxidase (NOX) 2 and NOX 4, with accelerated progression of atherosclerosis and acute coronary syndrome. Similar mechanisms of increased oxidative stress have also been associated with vasoconstriction and thrombosis. Furthermore, auto-phagosome function by lysosomes during cardiac arrest and return of spontaneous circulation (CA-ROSC) has proven to be impaired due to ROS dysregulating Beclin-1 and lysosomal-associated membrane protein 2 (LAMP2) following sudden cardiac events. Thus, minimizing levels of ROS can potentially prevent, reduce, and minimize myocardial injury. This understanding of ROS in biomedicine guides innovative therapies to restore redox balance and reduce the detrimental effects of oxidative stress.
Methods: We systematically reviewed over 30 recent and pertinent studies on reactive oxygen species (ROS) in cardiovascular diseases, employing diverse online databases, including PubMed, Google Scholar, and Web of Science. Our objective was to consolidate crucial findings from the most recent research, forming a comprehensive framework that encompasses the current understanding of the involvement of ROS in cardiac disorders. It is noteworthy that all statistical analyses cited in the literature were conducted by the respective authors of the individual studies.
Results: Reactive oxygen species (ROS) play a crucial role in cell signaling, immune response, and gene expression. However, an excess of ROS can result in oxidative stress and cellular dysfunction. This stress disrupts intracellular processes such as programmed cell death, downstream signaling, and cellular proliferation. Consequently, tissues experiencing oxidative stress undergo alterations in their regular functioning, leading to the development of diseases. In the pathogenesis of coronary heart disease, ROS are significant contributors, influencing hypertension, atherosclerosis, and thrombosis, all of which contribute to the likelihood of acute coronary syndrome. ROS production modifies LDL, causing the formation of atherosclerotic plaques. Increased ROS production in vascular smooth muscle cells and impaired endothelial function promote the development of atherosclerosis. Additionally, elevated glucose levels facilitate the formation of platelet-monocyte aggregates in diabetic patients, thereby increasing the risk of coronary artery disease.
Conclusions: This study emphasizes the crucial involvement of reactive oxygen species (ROS) in diverse cellular mechanisms, encompassing cell signaling, immune response, and gene expression. Nevertheless, an overabundance of ROS can trigger oxidative stress, perturbing vital intracellular functions and paving the way for cardiac diseases, ultimately culminating in acute coronary syndrome. Promising therapeutic approaches, such as polyphenols and ROS scavengers, present potential avenues for alleviating oxidative stress by modulating these physiological mechanisms.