Diabetes fuels periodontal lesions via GLUT1-driven macrophage inflammaging.
10.1038/s41368-021-00116-6
- Author:
Qian WANG
1
;
Lulingxiao NIE
1
;
Pengfei ZHAO
1
;
Xinyi ZHOU
1
;
Yi DING
1
;
Qianming CHEN
1
;
Qi WANG
2
Author Information
1. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & West China Hospital of Stomatology, Sichuan University, Chengdu, China.
2. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & West China Hospital of Stomatology, Sichuan University, Chengdu, China. wqinno8751@gmail.com.
- Publication Type:Research Support, Non-U.S. Gov't
- MeSH:
Animals;
Cellular Senescence;
Diabetes Mellitus, Experimental;
Glucose Transporter Type 1;
Inflammation;
Macrophages;
Mice
- From:
International Journal of Oral Science
2021;13(1):11-11
- CountryChina
- Language:English
-
Abstract:
Hyperglycemia induces chronic low-grade inflammation (inflammaging), which is a newly identified contributor to diabetes-related tissue lesions, including the inflammatory bone loss in periodontitis. It is also a secondary senescent pattern mediated by an increased burden of senescent cells and senescence-associated secretory phenotype (SASP). Macrophage is a key SASP-spreading cell and may contribute to the maintenance of SASP response in the periodontal microenvironment. Using a transgenic diabetic model (BLKS/J-Lepr
