Diabetic wound is one of the most refractory complications in diabetes mellitus, which can cause enormous economic, social, and public health burdens. Approximately 15% to 25% of patients with diabetes will develop at least one foot ulcer during their lifetime. The normal wound healing includes four programmed phases: hemostasis, inflammation, proliferation, and remodeling, though these phases are continuous and overlapped. However, diabetes results in delayed wound healing via multifarious biological mechanisms, which affect the transition of the organized phases. Up to now, a series of mechanisms comprising disordered growth factor production, impaired angiogenesis, imbalanced lymphocyte proliferation, and macrophage dysfunction may contribute to the delayed diabetic wound healing. These biological factors, immune cells, and signal pathways may become the potential targets for the therapeutic intervention.
Conventional therapeutic strategies of diabetic wound include glucose and infection control, debridement, wound off-loading, dressings, and revascularization. However, many of diabetic wounds are refractory to current treatments and fail to heal, persist for months or years, ultimately lead to amputation. It is a significant issue to develop a prompt, effective, and economic treatment of diabetic wound. For example, autologous platelet-rich plasma (PRP) is applied more and more widely to treat chronic/refractory wounds in clinic.
This Research Topic welcomes original research articles, clinical trials, case report, reviews, short communications, and commentaries on the potential mechanism of delayed diabetic wound healing. In addition, we encourage the exploration about some new therapeutic strategies targeting at these mechanisms, such as exogenous growth factors (PRP), agents restoring the dysregulated immune/inflammatory responses, bioengineered skin substitutes, and stem/progenitor cells.
Diabetic wound is one of the most refractory complications in diabetes mellitus, which can cause enormous economic, social, and public health burdens. Approximately 15% to 25% of patients with diabetes will develop at least one foot ulcer during their lifetime. The normal wound healing includes four programmed phases: hemostasis, inflammation, proliferation, and remodeling, though these phases are continuous and overlapped. However, diabetes results in delayed wound healing via multifarious biological mechanisms, which affect the transition of the organized phases. Up to now, a series of mechanisms comprising disordered growth factor production, impaired angiogenesis, imbalanced lymphocyte proliferation, and macrophage dysfunction may contribute to the delayed diabetic wound healing. These biological factors, immune cells, and signal pathways may become the potential targets for the therapeutic intervention.
Conventional therapeutic strategies of diabetic wound include glucose and infection control, debridement, wound off-loading, dressings, and revascularization. However, many of diabetic wounds are refractory to current treatments and fail to heal, persist for months or years, ultimately lead to amputation. It is a significant issue to develop a prompt, effective, and economic treatment of diabetic wound. For example, autologous platelet-rich plasma (PRP) is applied more and more widely to treat chronic/refractory wounds in clinic.
This Research Topic welcomes original research articles, clinical trials, case report, reviews, short communications, and commentaries on the potential mechanism of delayed diabetic wound healing. In addition, we encourage the exploration about some new therapeutic strategies targeting at these mechanisms, such as exogenous growth factors (PRP), agents restoring the dysregulated immune/inflammatory responses, bioengineered skin substitutes, and stem/progenitor cells.
