Terry Moore receives new R01 grant
Terry Moore, along with his co-Is Luisa DiPietro (Periodontics), Seungpyo Hong (U Wisconsin), and Sekhar Reddy (Pediatrics), received funding from the NIH/NIAMS for his project "Non-covalent Nrf2 Activators for the Treatment of Chromic Wounds". This grant is Dr. Moore's first R01 as an assistant professor her at UIC!
Dr. Moore's research will focus on chronic, non-healing wounds of the skin, which are serious medical complications that affect over 6.5 million Americans, particularly older adults. These wounds include pressure sores, diabetic foot ulcers, and venous ulcers. While there are numerous surgical and dressing treatments for these wounds, they still cause over 70,000 lower-limb amputations each year, and so it is clear that new treatments are needed. Strikingly, there are almost no pharmaceutical therapies to accelerate healing of chronic wounds. A major contributor to chronic wounds is a prolonged inflammatory state, and therefore reducing inflammation may be a way to accelerate healing of chronic wounds. Unfortunately, many commonly used anti-inflammatory drugs hinder chronic wound healing; thus, new ways of reducing inflammation are needed.
An essential factor in wound healing and an important regulator of inflammation is Nrf2, a transcription factor that induces many cytoprotective and antioxidant genes. As seen in other inflammatory disorders, activating Nrf2 could be a useful therapeutic strategy to treat chronic skin wounds. There are a number of covalent Nrf2 activators, but they are not selective for Nrf2, which is problematic because some of the off-target effects of these molecules are at proteins that hinder chronic wound healing. The central hypothesis of the Moore lab project is that pharmacologic activation of Nrf2 with non-covalent small molecules will accelerate wound healing, which could lead to new therapeutics to treat chronic wounds. Dr. Moore aims to find non-covalent activators of Nrf2, because they are likely more selective than non-electrophilic activators. Non-covalent Nrf2 activators can be developed by inhibiting the interaction of Nrf2 with its negative regulator, Keap1.