The overall significance of Core B is that it will provide standardized and rigorous bioinformatics and computational modeling analyses of all the molecular changes that occur in thoracic aortic aneurysms. Such analyses will allow each of the projects to develop a mechanistic understanding of the molecular changes that occur and how these changes contribute to the progression towards dissection. We anticipate such integrated analyses will help us deconvolute how multiple chemical signals as well as physical forces interact to control functions in the cells of the vessel wall during disease origin and progression.
There is substantial evidence that thoracic aortic aneurysms are a reflection of abnormal interactions of cells in the aortic media and their environment including both matrix and pressure. In this application we will define the mechanisms controlling these reactions with the intent of discovering novel points for therapeutic intervention. Core B will provide support thorough analysis of gene expression patterns for the construction of regulatory networks and development of models of select pathways and subnetworks from receptors to effector molecules.
| Bersi, Matthew R; Bellini, Chiara; Humphrey, Jay D et al. (2018) Local variations in material and structural properties characterize murine thoracic aortic aneurysm mechanics. Biomech Model Mechanobiol : |
| Latorre, Marcos; Humphrey, Jay D (2018) Modeling mechano-driven and immuno-mediated aortic maladaptation in hypertension. Biomech Model Mechanobiol : |
| Korneva, A; Zilberberg, L; Rifkin, D B et al. (2018) Absence of LTBP-3 attenuates the aneurysmal phenotype but not spinal effects on the aorta in Marfan syndrome. Biomech Model Mechanobiol : |
