posted on 2017-10-27, 00:00authored bySara M Fagen
A large number of publications now document alterations in wound healing phenotypes in genetically deficient or “knockout” mice. These studies have produced a disorganized dataset that describes the function of the specific genes in wound healing. To identify publications that describe wound healing phenotypes in knockout mice, a PubMed Literature search (1989-2016) was performed to identify manuscripts that examined in vivo excisional or incisional dermal wound healing in a genetically deficient mouse model. An electronic database was developed with standardized information for each publication. The database describes the specific parameters examined in each study including wound closure, cellular proliferation, immune response, angiogenesis, scarring, and the production of proteins/mediators.
The literature search resulted in the identification of 424 suitable manuscripts. Of those examining wound closure, 58.6% demonstrated a decrease in closure rates in the deficient mice, 18% demonstrated an increase, and 23.4% showed no change in the wound closure.
These results demonstrate that studies of wound healing in genetically deficient mice vary greatly in their specific healing parameters. We hypothesize that there are a variety of pathways affected, relating to cytokines and growth factor signaling. The development of a searchable database will support the identification of genetic elements related to specific wound healing phenotypes, and of groups of genes with common functions in wounds. In addition, the pathway analysis of this database may uncover gaps in our understanding of the healing process, and may suggest areas in which further research is needed.