.png){kind=icon}
.png){kind=icon}
Return
XBP1-mediated mitochondrial damage activates the mtDNA/STING/NLRP3 pathway to delay diabetic wound healing
.png){kind=icon}
OA
AI
M
Y
L
N
Z
C
W
S
Z
G
DOI：10.1097/CM9.0000000000004113.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Diabetic wounds (DBW) are characterized by high levels of reactive oxygen species (ROS) and pro-inflammatory factors; reducing inflammation is therefore a key strategy in the treatment of chronic diabetic wounds. X-box binding protein-1 (XBP1), a crucial transcription factor activated during endoplasmic reticulum stress, has been found to mediate mitochondrial damage, thereby activating the mitochondrial deoxyribonucleic acid/cyclic GMP-AMP synthase/stimulator of interferon genes (mtDNA/cGAS/STING) pathway and inducing Kupffer cell M1 polarization, which leads to excessive secretion of inflammatory cytokine. However, its role in regulating DBW healing remains unclear. Therefore, this study aims to explore the underlying mechanism of XBP1 in diabetic wound healing.
Keywords:
X-box binding protein-1
Diabetic wound healing
Mitochondrial deoxyribonucleic acid
cGAS/STING pathway
NOD-
LRR- and pyrin domain-containing protein 3
Journal
IF:
7.3
Papers:
1.2W
Citations:
1.5W
Organization
Cited Papers