RESUMO
Significance: The incidence of pressure ulcers is increasing due to our aging population and the increase in the elderly living with disability. Learning how to manage pressure ulcers appropriately is increasingly important for all professionals in wound care. Recent Advances: Many new dressings and treatment modalities have been developed over the recent years and the goal of this review is to highlight their benefits and drawbacks to help providers choose their tools appropriately. Critical Issues: Despite an increased number of therapies available on the market, none has demonstrated any clear benefit over the others and pressure ulcer treatment remains frustrating and time-consuming. Future Directions: Additional research is needed to develop products more effective in prevention and treatment of pressure ulcers.
RESUMO
Current knowledge of wound healing is based on studies using various in vitro and in vivo wound models. In vitro models allow for biological examination of specific cell types involved in wound healing. In vivo models generally provide the full spectrum of biological responses required for wound healing, including inflammation and angiogenesis, and provide cell-cell interactions not seen in vitro. In this review, the authors aim to delineate the most relevant wound healing models currently available and to discuss their strengths and limitations in their approximation of the human wound healing processes to aid scientists in choosing the most appropriate wound healing models for designing, testing, and validating their experiments.
Assuntos
Cicatrização/fisiologia , Animais , Células Cultivadas , Humanos , Modelos AnimaisRESUMO
Wound healing is characterized by the production of large amounts of protein necessary to replace lost cellular mass and extracellular matrix. The unfolded protein response (UPR) is an important adaptive cellular response to increased protein synthesis. One of the main components of the UPR is IRE1, an endoplasmic reticulum transmembrane protein with endonuclease activity that produces the activated form of the transcription factor XBP1. Using luciferase reporter mice for Xbp1 splicing, we showed that IRE1 was up-regulated during excisional wound healing at the time in wound healing consistent with that of the proliferative phase, when the majority of protein synthesis for cellular proliferation and matrix deposition occurs. Furthermore, using a small molecule inhibitor of IRE1 we demonstrated that inhibition of IRE1 led to decreased scar formation in treated mice. Results were recapitulated in a hypertrophic scar mouse model. These data help provide a cellular pathway to target in the treatment of hypertrophic scarring and keloid disorders.