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Dr. Rubin is a basic scientist whose research has always focused on understanding cellular signaling pathways. She began her research career at MU exploring second messenger signaling involved in control of cardiovascular function. Rodent models were employed to explore how immune mediators, released during inflammatory conditions (endotoxemia/sepsis) cause myocardial failure and/or vascular dysfunction through modulation of the activity of specific cellular targets such as potassium and calcium channels or contractile proteins. More recent work explored the signaling mechanism impacted by specific therapeutic modalities such as the anesthetic, ketamine which appears able to protect cardiovascular function during inflammatory states. Related studies utilized a swine model of atherosclerosis and the influence of gender to determine whether exercise had beneficial effects on receptor mediated signaling pathways and function of coronary smooth muscle. Studies that explored cellular signaling pathways involved in vascular metabolic vasodilation which is essential to match blood flow to tissue energy demands during exercise or disease impairment led the research to examine the role of AMP kinase, then a novel signaling pathway. Dr. Rubin’s studies were the first to explore the role of AMPK in vascular smooth muscle function and metabolic vasodilation. These studies continue in the laboratory with the addition of the AMPK knock out mouse model. A serendipitous finding for this model was an interaction between AMPK alpha-1 KO and the C57Bl6 mouse strain which presents with significant cardiac hypertrophy that resembles physiologic hypertrophy. Current and future studies are directed at understanding the signaling pathway impacted by this interaction to better understand the cellular pathways that underlie exercise and disease-induced cardiac hypertrophy.
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Medicine & Science in Sports & Exerciseno. 5S (2018): 541-542
Medicine and Science in Sports and Exercise (2018): 541-542
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