Peripheral origin exosomal microRNAs aggravate glymphatic system dysfunction in diabetic cognitive impairment.
10.1016/j.apsb.2023.03.018
- Author:
Lin ZHANG
1
;
Dongna LI
1
;
Pengrong YI
1
;
Jiangwei SHI
2
;
Mengqing GUO
1
;
Qingsheng YIN
1
;
Dingbin LIU
3
;
Pengwei ZHUANG
1
;
Yanjun ZHANG
1
Author Information
1. State Key Laboratory of Component-based Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China.
2. First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.
3. State Key Laboratory of Medicinal Chemical Biology, Research Center for Analytical Sciences, and Tianjin Key Laboratory of Molecular Recognition and Biosensing, College of Chemistry, Nankai University, Tianjin 300071, China.
- Publication Type:Review
- Keywords:
AQP4;
Astrocyte;
Central nervous system;
Diabetes mellitus;
Diabetic cognitive impairment;
Exosomal miRNAs;
Glymphatic system;
Peripheral–central communication
- From:
Acta Pharmaceutica Sinica B
2023;13(7):2817-2825
- CountryChina
- Language:English
-
Abstract:
Cognitive dysfunction is one of the common central nervous systems (CNS) complications of diabetes mellitus, which seriously affects the quality of life of patients and results in a huge economic burden. The glymphatic system dysfunction mediated by aquaporin-4 (AQP4) loss or redistribution in perivascular astrocyte endfeet plays a crucial role in diabetes-induced cognitive impairment (DCI). However, the mechanism of AQP4 loss or redistribution in the diabetic states remains unclear. Accumulating evidence suggests that peripheral insulin resistance target tissues and CNS communication affect brain homeostasis and that exosomal miRNAs are key mediators. Glucose and lipid metabolism disorder is an important pathological feature of diabetes mellitus, and skeletal muscle, liver and adipose tissue are the key target insulin resistance organs. In this review, the changes in exosomal miRNAs induced by peripheral metabolism disorders in diabetes mellitus were systematically reviewed. We focused on exosomal miRNAs that could induce low AQP4 expression and redistribution in perivascular astrocyte endfeet, which could provide an interorgan communication pathway to illustrate the pathogenesis of DCI. Furthermore, the mechanisms of exosome secretion from peripheral insulin resistance target tissue and absorption to the CNS were summarized, which will be beneficial for proposing novel and feasible strategies to optimize DCI prevention and/or treatment in diabetic patients.
