Review
Version 1
This version is not peer-reviewed
Vascular Nadph Oxidases and Atherothrombotic Stroke
Version 1
: Received: 26 July 2024 / Approved: 26 July 2024 / Online: 26 July 2024 (12:48:23 CEST)
How to cite: Marqués, J.; Zalba, G. Vascular Nadph Oxidases and Atherothrombotic Stroke. Preprints 2024, 2024072171. https://doi.org/10.20944/preprints202407.2171.v1 Marqués, J.; Zalba, G. Vascular Nadph Oxidases and Atherothrombotic Stroke. Preprints 2024, 2024072171. https://doi.org/10.20944/preprints202407.2171.v1
Abstract
Oxidative stress constitutes a main molecular mechanism underlying cardiovascular diseases (CVDs). This pathological mechanism can be triggered by NADPH oxidases (NOXs), which produce reactive oxygen species (ROS). In fact, the different NOXs have been associated with myocardial infarction, atherothrombosis, and stroke. More specifically, we will focus on the implications of NOXs in atherothrombotic stroke. Each NOX member participates in a different way in the several stages of this disease: endothelial dysfunction, immune cell infiltration, foam cell genesis, vascular smooth muscle cells (VSMC) proliferation, and atherosclerotic plaque formation. Additionally, some NOXs are involved in plaque instability, thrombosis, ischemic stroke, and ischemia-reperfusion injury (IRI). Interestingly, the effects of NOXs in this pathology depend on the specific homologue, the cell type in which they are activated, and the stage of the disease. In this review we summarize the most up-to-date information about the implications of vascular NOXs in each of these processes. Finally, we highlight some limitations and future perspectives of the study of NOXs in CVDs.
Keywords
Oxidative stress; NADPH oxidases; NOX; atherosclerosis; thrombosis; stroke; vessel wall; atherothrombosis
Subject
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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