Why should we explore the effect of inflammation-induced oxidative stress in the aortic heart valve of diabetic individuals?
Currently, the only effective CAVD treatment is valve replacement.
The bioprosthetic valves are last ~10-15 years in the general population, but only 5-7 years in diabetic patients
Given this information, our team performed a literature review researching several hyperglycemic induced pathways leading to calcification
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O-linked β-N-acetylglucosamine (O-GlcNAc)
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Inflammation
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Oxidative Stress
In this we defined that inflammation and oxidative stress interact via a feedback loop
This brings us to our overarching research goal:
Investigate the connection between glucose and calcification.
Objective 1
Measure TNF-α production under hyperglycemic conditions.
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Hypothesis
TNF-α production will increase in endothelial cells cultured in hyperglycemic conditions.
Objective 2
Quantify ROS and RNS levels to assess oxidative stress.
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Hypothesis
ROS will increase and RNS will decrease in endothelial cells cultured in high glucose
Objective 1
Determine Calcification with/without:
TNF-a inhibitors, ROS Scavengers, Supplemental NO
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Hypothesis
TNF-α inhibitors, ROS scavengers, and supplemental NO will reduce calcification in endothelial cells in high glucose.
Meet the Team
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Dr. Alysa
Morss Clyne
Team Faculty Mentor
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Nedelina Tchangalova
Team Librarian
Malavika Kattuparambil
Team Liaison
Neuroscience
Neha
Neelam
Mentor Liaison
Psychology
Maddie Paritsky
Ombudsperson
Neurobiology and Physiology
Sophia Brandon
Web Liaison
Bioengineering
Nick
Santiago
Library Liaison
Neuroscience
Natalia Martinez
Team Clerk
General Biology
Manvi Kalachagari
Team Clerk
Public Health
Isabelle
George
Lab Coordinator
Public Health & Art History
Anita
Ma
Financial Liaison
General Biology
Iris
Kalfa
Financial Liaison
Neuroscience