Presentation Type

Thesis

Department

Biology

Location

Walker Conference Center C

Description

Atherosclerosis is a disease of the cardiovascular system that is characterized by the buildup of plaque inside arteries over several decades. These plaques have the potential to rupture, causing a clot to form in the vessel. This results in an acute cardiovascular event such as myocardial infarction or stroke. Atherosclerosis remains a significant public health challenge in developed countries, being the foundational cause of roughly 50% of deaths in westernized societies and a major contributor to health costs [13,14]. Understanding this devastating disease and developing preventative measures is a highly important area of research. While the impact of cardiovascular disease is often associated with adulthood, the process of atherosclerosis, a key precursor to many cardiovascular events, initiates as early as the first decade of life [14]. Studies have demonstrated that the severity of atherosclerosis is intricately linked to genetic risk factors and the number and intensity of external risk factors such as lifestyle or nutrition [14]. These risk factors can manifest and accumulate from childhood, influencing the trajectory of cardiovascular health throughout a person's life [14]. The early detection of cardiovascular risk factors in children is paramount, as it provides a crucial opportunity to implement interventions and lifestyle modifications to protect against this devastating disease [14]. Early detection is vital not only for preventing immediate health threats but also in mitigating the long-term burden and associated costs of treating cardiovascular diseases in our health system. Recent research suggests that platelets may play a pivotal role in the development of several diseases, including atherosclerosis [2]. Platelets are small, anucleate, cell fragments that are crucial for hemostasis. These cell fragments also have the ability to respond to stress and contribute to physiological processes including immunoregulation and wound healing [2]. Platelets are involved in the early development of atherosclerotic disease through the recruitment of leukocytes to the endothelium and promotion of a pro-inflammatory environment, additionally playing a role in the inflammatory response [2,10]. Platelets are highly active metabolically and require a high rate of ATP turnover, making platelet mitochondria vital to maintain these appropriate physiological functions [1,2]. The health of the platelet has been shown to be determined largely by the health of their mitochondria, with platelet mitochondrial dysfunction resulting in reduction in platelet survival and an increased risk of thrombovascular events [2]. Because of the role held by platelets in the development of atherosclerosis and the importance of their mitochondria, analysis of platelet mitochondrial bioenergetics may serve as an early marker or a ‘canary in the coal mine’ for chronic cardiovascular disease [6]. Analysis of platelet mitochondrial function is done through cellular mitochondrial function assay, providing a set of parameters that offer insights into various facets of mitochondrial function [6]. Mitochondrial function assay captures oxygen consumption rates (OCR) across the mitochondria including ATP-linked OCR, OCR due to proton leak, maximal OCR, basal OCR, reserve capacity, coupling efficiency, and non-mitochondrial OCR [6]. These parameters, when considered collectively, can be utilized to calculate the Bioenergetic Health Index (BHI), a measure of metabolic health [6]. Generally, malfunctions in the Electron Transport Chain can lead to a reduced BHI due to lower reserve capacity, ATP-linked respiration, or increased uncoupling due to higher proton leak across the inner mitochondrial membrane. The BHI identifies a gradual decline in bioenergetic health before the cell reaches the threshold of energy demand failure. The obtained values have the potential to indicate the well-being of mitochondria within platelets, reflecting the overall health of the platelet and possibly atherosclerotic disease risk and progression [6].

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Apr 24th, 4:30 PM Apr 24th, 4:45 PM

Peak Aerobic Capacity and Dietary Composition are Associated with the Bioenergetic Profile of Platelets in Children

Walker Conference Center C

Atherosclerosis is a disease of the cardiovascular system that is characterized by the buildup of plaque inside arteries over several decades. These plaques have the potential to rupture, causing a clot to form in the vessel. This results in an acute cardiovascular event such as myocardial infarction or stroke. Atherosclerosis remains a significant public health challenge in developed countries, being the foundational cause of roughly 50% of deaths in westernized societies and a major contributor to health costs [13,14]. Understanding this devastating disease and developing preventative measures is a highly important area of research. While the impact of cardiovascular disease is often associated with adulthood, the process of atherosclerosis, a key precursor to many cardiovascular events, initiates as early as the first decade of life [14]. Studies have demonstrated that the severity of atherosclerosis is intricately linked to genetic risk factors and the number and intensity of external risk factors such as lifestyle or nutrition [14]. These risk factors can manifest and accumulate from childhood, influencing the trajectory of cardiovascular health throughout a person's life [14]. The early detection of cardiovascular risk factors in children is paramount, as it provides a crucial opportunity to implement interventions and lifestyle modifications to protect against this devastating disease [14]. Early detection is vital not only for preventing immediate health threats but also in mitigating the long-term burden and associated costs of treating cardiovascular diseases in our health system. Recent research suggests that platelets may play a pivotal role in the development of several diseases, including atherosclerosis [2]. Platelets are small, anucleate, cell fragments that are crucial for hemostasis. These cell fragments also have the ability to respond to stress and contribute to physiological processes including immunoregulation and wound healing [2]. Platelets are involved in the early development of atherosclerotic disease through the recruitment of leukocytes to the endothelium and promotion of a pro-inflammatory environment, additionally playing a role in the inflammatory response [2,10]. Platelets are highly active metabolically and require a high rate of ATP turnover, making platelet mitochondria vital to maintain these appropriate physiological functions [1,2]. The health of the platelet has been shown to be determined largely by the health of their mitochondria, with platelet mitochondrial dysfunction resulting in reduction in platelet survival and an increased risk of thrombovascular events [2]. Because of the role held by platelets in the development of atherosclerosis and the importance of their mitochondria, analysis of platelet mitochondrial bioenergetics may serve as an early marker or a ‘canary in the coal mine’ for chronic cardiovascular disease [6]. Analysis of platelet mitochondrial function is done through cellular mitochondrial function assay, providing a set of parameters that offer insights into various facets of mitochondrial function [6]. Mitochondrial function assay captures oxygen consumption rates (OCR) across the mitochondria including ATP-linked OCR, OCR due to proton leak, maximal OCR, basal OCR, reserve capacity, coupling efficiency, and non-mitochondrial OCR [6]. These parameters, when considered collectively, can be utilized to calculate the Bioenergetic Health Index (BHI), a measure of metabolic health [6]. Generally, malfunctions in the Electron Transport Chain can lead to a reduced BHI due to lower reserve capacity, ATP-linked respiration, or increased uncoupling due to higher proton leak across the inner mitochondrial membrane. The BHI identifies a gradual decline in bioenergetic health before the cell reaches the threshold of energy demand failure. The obtained values have the potential to indicate the well-being of mitochondria within platelets, reflecting the overall health of the platelet and possibly atherosclerotic disease risk and progression [6].

 

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