| Literature DB >> 28419584 |
Francesco Vieceli Dalla Sega1, Giorgio Aquila1, Francesca Fortini1, Mauro Vaccarezza2, Paola Secchiero3,4, Paola Rizzo3,5, Gianluca Campo1,6.
Abstract
Reactive oxygen species (ROS) act as signal molecules in several biological processes whereas excessive, unregulated, ROS production contributes to the development of pathological conditions including endothelial dysfunction and atherosclerosis. The maintenance of a healthy endothelium depends on many factors and on their reciprocal interactions; in this framework, the Notch pathway and shear stress (SS) play two lead roles. Recently, evidence of a crosstalk between ROS, Notch, and SS, is emerging. The aim of this review is to describe the way ROS interact with the Notch pathway and SS protecting from-or promoting-the development of endothelial dysfunction.Entities:
Keywords: Notch; ROS; endothelial dysfunction; shear stress
Mesh:
Substances:
Year: 2017 PMID: 28419584 DOI: 10.1002/biof.1359
Source DB: PubMed Journal: Biofactors ISSN: 0951-6433 Impact factor: 6.113