氧化应激
炎症
NF-κB
伤口愈合
活性氧
药理学
信号转导
医学
糖尿病
微泡
NFKB1型
生物信息学
化学
细胞生物学
生物
内科学
免疫学
内分泌学
转录因子
小RNA
生物化学
基因
作者
Feiyu Cai,Wenjiao Chen,Ruomei Zhao,Yi Liu
标识
DOI:10.1007/s11033-023-08392-7
摘要
The issue of delayed wound healing or nonhealing in diabetic patients presents a challenge for modern medicine. A number of attempts have been made to understand the mechanisms behind diabetic wound. In a hyperglycemic environment, increased intracellular reactive oxygen species (ROS) disturb the balance between oxidation and antioxidant, causing the wound environment to deteriorate. It has been established that the nuclear factor E2-related factor 2 (Nrf2) and nuclear factor-kappa B (NF-κB) pathways play an important role in regulating inflammation and oxidative stress. Several potential treatment strategies involving Nrf2 and/or NF-κB pathways have been explored in previous studies. Hence, we analyzed mechanisms and changes in Nrf2 and NF-κB pathways in response to oxidative stress and inflammation in diabetic environment. Additionally, we reviewed potential treatment strategies from the past five years for diabetic wound by Nrf2 and/or NF-κB pathways, including receptor agonists, vitamins, hormones, exosomes, drugs, plants, and biomaterials. It may be useful to develop drugs to promote diabetic wound healing.
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