Abstract：
Diabetic wounds are slow healing wounds characterized by disordered healing processes and frequently take longer than three months to heal. One of the defining characteristics of impaired diabetic wound healing is an abnormal and unresolved inflammatory response, which is primarily brought on by abnormal macrophage innate immune signaling activation. The persistent inflammatory state in a diabetic wound may be attributed to inflammatory pathways such as nuclear factor kappa B (NF-ĸB) and nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, which have long been associated with inflammatory diseases. Despite the available treatments for diabetic foot ulcers (DFUs) that include debridement, growth factor therapy, and topical anti-bacterial agents, successful wound healing is still hampered. Further understanding of the molecular mechanism of these pathways could be useful in designing potential therapeutic targets for diabetic wound healing. This review provides an update and novel insights into the roles of NF-ĸB and NLRP3 pathways in the molecular mechanism of diabetic wound inflammation and their potential as therapeutic targets in diabetic wound healing.
摘要：
糖尿病伤口是缓慢愈合的伤口,其特征在于无序的愈合过程,并且通常需要超过三个月的时间才能愈合。糖尿病伤口愈合受损的定义特征之一是异常和未解决的炎症反应，这主要是由异常巨噬细胞先天免疫信号激活引起的。糖尿病伤口中的持续炎症状态可能归因于炎症途径，例如核因子κB（NF-κB）和含节点样受体家族pyrin结构域3（NLRP3）炎症小体，长期以来与炎症性疾病有关。尽管糖尿病足溃疡（DFU）的可用治疗方法包括清创术，生长因子治疗,和局部抗菌剂，成功的伤口愈合仍然受到阻碍。进一步了解这些途径的分子机制可用于设计糖尿病伤口愈合的潜在治疗靶标。这篇综述为NF-κB和NLRP3通路在糖尿病伤口炎症的分子机制中的作用以及它们作为糖尿病伤口愈合治疗靶点的潜力提供了更新和新的见解。
