Correlation Engine 2.0
Clear Search sequence regions

Sizes of these terms reflect their relevance to your search.

The delayed repair process in the aging diabetic population is becoming an alarming public health concern. ICAM-1 plays an important role in orchestrating the repair process by mediating neutrophil recruitment and phagocytosis. However, little is known about the role of ICAM-1 in aging diabetic repair. By causing injury in aging diabetic mice with ICAM-1 deletion (AD-ICAM-1-/-), we found that AD-ICAM-1-/- mice exhibited a delayed repair process with incomplete re-epithelialization and reduced angiogenesis. Additionally, high-throughput Illumina sequencing was performed to evaluate the microbiota of such mice. The results indicate that the microbiota of the AD-ICAM-1-/- injury site differed taxonomically at both the phylum and genus levels. Neutrophil recruitment and phagocytic function were also reduced in the AD-ICAM-1-/- group. Notably, major inflammatory biomarker expression was also detected in AD-ICAM-1-/- injured tissue. Overall, this study demonstrated that AD-ICAM-1-/- mice exhibit delayed repair. In addition, neutrophil recruitment and phagocytic activity were impaired in the AD-ICAM-1-/- group, which may have allowed microbes to colonize the injury site. Copyright © 2020 Elsevier Inc. All rights reserved.


Dongxu Qiu, David Nikita, Lei Zhang, Jun Deng, Zhiwei Xia, Junkun Zhan, Jiabing Huang, Lanzhi Liu, Fan Liu, Jingfeng Duan, Jing Li. ICAM-1 deletion delays the repair process in aging diabetic mice. Metabolism: clinical and experimental. 2021 Jan;114:154412

Expand section icon Mesh Tags

Expand section icon Substances

PMID: 33164859

View Full Text