Key result
Excessive reactive oxygen species drive endothelial dysfunction, smooth muscle apoptosis, and vascular remodeling.
Why the study?
Growing evidence indicates that traditional risk factors translate into reactive oxygen species and contribute to vascular injury, vasculitis, and other vascular diseases.
This review summarizes the molecular mechanisms by which reactive oxygen species and oxidative stress contribute to atherosclerosis, aortic dissection, aortic aneurysm, and pulmonary arterial hypertension, highlighting potential antioxidant therapeutic targets.
Answers are grounded in this paper and cite their sources.
May guide antioxidant target selection in vascular disease; leaves open randomized confirmation of clinical benefit.
Oxidative stress (OS) refers to the enhancement of oxidation and the decreased of related antioxidant enzymes activity under pathological conditions, resulting in relatively excess reactive oxygen species (ROS), causing cytotoxicity, which leads to tissue damage and is linked to neurodegenerative diseases, cardiovascular diseases, diabetes, cancers, and many other pathologies. As an important intracellular signaling molecule, ROS can regulate numerous physiological actions, such as vascular reactivity and neuronal function. According to several studies, the uncontrolled production of ROS is related to vascular injury. The growing evidence revealing how traditional risk factors translate into ROS and lead to vasculitis and other vascular diseases. In this review, we sought to mainly discuss the role of ROS and antioxidant mechanisms in vascular-related diseases, especially cardiovascular and common macrovascular diseases.
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Cheng et al. (2022) conducted a review in Vascular-related diseases (atherosclerosis, aortic dissection, aortic aneurysm, and pulmonary arterial hypertension). Reactive oxygen species (ROS) and antioxidant mechanisms was evaluated. Excessive reactive oxygen species production and oxidative stress drive endothelial dysfunction, smooth muscle cell apoptosis, and extracellular matrix remodeling in vascular diseases.
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