Abstract
The nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) family is the major source of reactive oxygen species (ROS) in the vascular system. In this family, NOX4, a constitutive active form of NOXs, plays an important role in angiogenesis. Thioredoxin 2 (TRX2) is a key mitochondrial redox protein that maintains normal protein function and also provides electrons to peroxiredoxin 3 (PRX3) to scavenge H2O2 in mitochondria. Angiogenesis, a process of new blood vessel formation, is involved in a variety of physiological processes and pathological conditions. It seems to be paradoxical for ROS-producing NOX4 and ROS-scavenging TRX2 to have a similar role in promoting angiogenesis. In this review, we will focus on data supporting the role of NOX4 and TRX2 in angiogenesis and their cross-talks and discuss how ROS can positively or negatively regulate angiogenesis, depending on their species, levels and locations. NOX4 and TRX2-mediated ROS signaling could be promising targets for the treatment of angiogenesis-related diseases.
Highlights
Angiogenesis, a process of new blood vessel formation, is involved in a variety of physiological processes and pathological conditions [1,2,3]
The aim of this review is to briefly summarize recent progress and information on the redox signaling in angiogenesis with a focus on NOX4 and Thioredoxin 2 (TRX2)
Compelling evidence demonstrates that NOX4 and its generated H2 O2 play an important role in cell proliferation, migration, apoptosis and oxygen sensing, which has been reviewed in detail elsewhere [28]
Summary
Angiogenesis, a process of new blood vessel formation, is involved in a variety of physiological processes and pathological conditions [1,2,3]. Recent reports suggest that ROS generated from mitochondria gravely regulate endothelial cell (EC) function [2,3,7,8]. ROS are known to serve as second messengers in signal transduction that regulate EC growth, proliferation, apoptosis, barrier function, vasodilatation and vascular remodeling [9,10,11]. This is well demonstrated from in vitro hypoxia and in vivo ischemia on angiogenesis. Excessive ROS production resulting from mitochondrial dysfunction can inhibit reparative angiogenesis by inducing endothelial dysfunction and cell apoptosis under pathological conditions such as diabetes and myocardial infarction. The aim of this review is to briefly summarize recent progress and information on the redox signaling in angiogenesis with a focus on NOX4 and TRX2
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