Grants We Funded
Grant applicants for the 2022 cycle requested a total of over $2.9 million dollars. The PSF Study Section subcommittees of Basic & Translational Research and Clinical Research evaluated 115 grant applications on the following topics:
The PSF awarded research grants totaling almost $550,000 to support 19 plastic surgery research proposals.
ASPS/PSF leadership is committed to continuing to provide high levels of investigator-initiated research support to ensure that plastic surgeons have the needed research resources to be pioneers and innovators in advancing the practice of medicine.
Search The PSF database to have easy access to full-text grant abstracts from past PSF-funded research projects 2003 to present. All abstracts are the work of the Principal Investigators and were retrieved from their PSF grant applications. Several different filters may be applied to locate abstracts specific to a particular focus area or PSF funding mechanism.
Macrophage Dysfunction in Diabetic Wound Healing
Mimi Leong MD
Baylor College of Medicine
Basic Research Grant
Normal wound healing is characterized by three phases: inflammation, proliferation, and maturation (remodeling). Angiogenesis, the process of new blood vessel formation, is an important component of the proliferative phase of wound healing and is crucial to support the healing wound environment. Chronic wounds, such as diabetic wounds, fail to complete all stages of wound healing; these wounds are likely ischemic in nature as hypoxia and inflammation play key roles in their failure to progress to healing. Macrophages secrete numerous growth factors and mediators vital to all phases of wound healing, particularly the inflammatory and proliferative phases. In chronic wounds, however, macrophages appear to be senescent (Moore, 1997), staying at the wound edge. This altered chemotaxis may be a result of the accumulation of advanced glycation end-products (AGEs) within diabetic skin (Goova, 2001). Elevated levels of AGEs and the concomitant increased expression of receptor for advanced glycation end-products (RAGE), lead to increased free radical formation and inflammatory cytokine production (Simm, 2004). Wound healing studies have suggested that the nonhealing diabetic wound is in a pro-inflammatory state. Subsequently, we hypothesize that increased expression of RAGE results in wound macrophage dysfunction by decreasing macrophage-mediated angiogenesis and prolonging macrophage-mediated inflammation.