In human tissue repair process, fibrous tissues will be rapidly generated to replace wounded tissues. Over-repairing of wounded tissues could result in tissue fibrosis, chronic inflammation, damage of epithelial and endothelial cells, and excessive proliferation of fibroblasts. The excessive collagen accumulation forms large amounts of fibrous tissue, which may cause failure and increase the risk of cancer. In this study, we integrated various important signaling pathways involved in human tissue repair and fibrosis, and established a signaling pathway model of Thrombin-activated CTGF expression. Based on Mass Action Law, continuum hypothesis, and well-mixed assumption, we built a quantitative, computable ODE model of the signaling pathway in order to explore the dynamic responses and operating points of the pathway. From studying the CTGF promoter regulations, we aim to find ways to reduce or delay tissue fibrosis and aging due to tissue over-repairing after damage, and hence to reduce the risk of cancer and to facilitate drug development of preventing tissue fibrosis.
|Effective start/end date||8/1/14 → 7/31/15|
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