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Modeling Smoking Induced Cardiac Dysfunction in 3D Microtissues

Institution: Stanford University
Investigator(s): Dilip Thomas,
Award Cycle: 2019 (Cycle 29) Grant #: T29FT0380 Award: $128,086
Subject Area: Cardiovascular and Cerebrovascular Disease
Award Type: Postdoctoral Fellowship Awards

Initial Award Abstract
Tobacco and nicotine-related harmful effects are major risk factors for premature cardiovascular diseases in both sexes around the world. Tobacco use is estimated to account for 7.2 million deaths in 2015 worldwide and approximately 480,000 per year in the United States alone. In addition to direct pulmonary damage caused by tobacco smoke, one of the main active ingredients, nicotine, affects the heart, liver and kidney due to its high concentration and residence in plasma. Approximately 10-15% of nicotine absorbed from a cigarette leads to tobacco-related systemic effects such as oxidative damage, inflammation and arrhythmogenesis, all of which promote progression toward heart failure. Heart tissues derived from smokers and non-smokers would serve as a useful surrogate to perform in vitro experiments to understand and define the pathogenic progression of tobacco-related cardiovascular disease. Because primary tissues are difficult to obtain and maintain in vitro, tissue engineered extracellular matrix (ECM)-based three-dimensional (3-D) tissue models that recapitulate cellular composition and microenvironment offer a promising alternative to assess functional abnormalities. The overall hypothesis of my TRDRP proposal is that 3-D extracellular matrix-based multicellular heart microtissues (MHMs) comprising human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes (CMs), endothelial cells (ECs), and cardiac fibroblast (CFs) can be utilized to model tobacco smoke induced cardiac dysfunction.