Why the study?
To provide an overview of the role of reactive oxygen species in human blood vessel physiology, specifically their interaction with the Renin-Angiotensin System and how RAS-targeting clinical interventions influence vascular redox signaling.
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Design
Review
This review highlights the interplay between the Renin-Angiotensin System and reactive oxygen species in vascular homeostasis and the mechanistic impact of RAS blockers on redox signaling.
Extensive research has been conducted to elucidate and substantiate the crucial role of the Renin-Angiotensin System (RAS) in the pathogenesis of hypertension, cardiovascular disorders, and renal diseases. Furthermore, the role of oxidative stress in maintaining vascular balance has been well established. It has been observed that many of the cellular effects induced by Angiotensin II (Ang II) are facilitated by reactive oxygen species (ROS) produced by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. In this paper, we present a comprehensive overview of the role of ROS in the physiology of human blood vessels, specifically focusing on its interaction with RAS. Moreover, we delve into the mechanisms by which clinical interventions targeting RAS influence redox signaling in the vascular wall.
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Κούμαλλος et al. (2023) studied this question.
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