Fibrosis is the histological manifestation of chronic kidney disease (CKD). While the kidney can fully regenerate and repair following acute kidney injury (AKI), injury response can also follow a maladapative path in fibrosis resulting in epithelial atrophy, accumulation of myofibroblasts, collagen and inflammatory cells. A key bottleneck to progress in our understanding of regeneration and differentiation has been the limited insight into cell-specific genome wide gene expression changes. A revolution in cellular measurement technology is under way. For the first time, we have the ability to monitor genome-wide gene regulation in thousands of individual cells in a single experiment, using single cell ?omic? studies. Such experiments allow us to discover new cell types and states, trace the origin of cells and identify underlying cell- specific gene expression changes therefore, this method shall enable us to understand reparative and maladaptive regeneration in fibrosis. The primary goal of this proposal is to explore the hypothesis that the Notch pathway plays an important role in the development of chronic kidney disease and kidney fibrosis.
One in ten Americans are affected by chronic kidney disease (CKD). CKD is a gene environmental disease. Critical cell type(s) and pathway(s) responsible for disease development remains unknown limiting CKD understanding and new therapeutics development.
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