Role of moesin, Src, and ROS in advanced glycation end product-induced vascular endothelial dysfunction.
Microcirculation
; 24(3)2017 04.
Article
en En
| MEDLINE
| ID: mdl-28129474
ABSTRACT
The disruption of endothelial integrity and the occurrence of angiogenesis in response to AGEs contribute greatly to micro- and macrovascular complications associated with DM. Among human dermal, brain, and retinal vascular ECs, activation of ERM, moesin, by phosphorylation of Thr-558 is involved in AGE-induced hyperpermeability and angiogenesis via the Rho and ROCK (Rho/ROCK) and p38 pathways. Src also plays an important role in AGE-induced endothelial barrier dysfunction by phosphorylating moesin, VE-cadherin, and FAK. Furthermore, recent studies have demonstrated that ROS serve as a key mediator of the AGE-induced endothelial response. ROS inhibition would greatly benefit ECs. This review focuses on the role of moesin in microvascular permeability and angiogenesis, and on the involvement of Src and ROS in endothelial barrier disruption.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Endotelio Vascular
/
Productos Finales de Glicación Avanzada
/
Proteínas de Microfilamentos
Límite:
Humans
Idioma:
En
Revista:
Microcirculation
Asunto de la revista:
ANGIOLOGIA
Año:
2017
Tipo del documento:
Article
País de afiliación:
China