Abstract
Accumulating evidence demonstrates that vascular oxidative stress is a critical feature of atherosclerotic process, potentially triggered by several infectious agents that are considered as risk co-factors for the atherosclerotic cardiovascular diseases (CVDs). C. pneumoniae has been shown to upregulate multiple enzymatic systems capable of producing reactive oxygen species (ROS) such as NADPH oxidase (NOX) and cyclooxygenase in vascular endothelial cells, NOX and cytochrome c oxidase in macrophages as well as nitric oxide synthase and lipoxygenase in platelets contributing to both early and late stages of atherosclerosis. P. gingivalis seems to be markedly involved in the atherosclerotic process as compared to A. actinomycetemcomitans contributing to LDL oxidation and foam cell formation. Particularly interesting is the evidence describing the NLRP3 inflammasome activation as a new molecular mechanism underlying P. gingivalis-induced oxidative stress and inflammation. Amongst viral agents, immunodeficiency virus-1 and hepatitis C virus seem to have a major role in promoting ROS production, contributing, hence, to the early stages of atherosclerosis including endothelial dysfunction and LDL oxidation. In conclusion, oxidative mechanisms activated by several infectious agents during the atherosclerotic process underlying CVDs are very complex and not well-known, remaining, thus, an attractive target for future research.
Highlights
Atherosclerotic cardiovascular diseases (CVDs) continue to represent a major public health problem in developed countries, accounting for one-third of all deaths worldwide [1]
We focus on the oxidative mechanisms through which infectious agents may contribute to the early stages of the atherosclerotic process, by promoting endothelial dysfunction, low-density lipoprotein (LDL) oxidation, and foam cell formation, and to the late stages, by stimulating platelet activation and vascular smooth muscle cell (VSMC) migration and proliferation
Green tea epigallocatechin-3-gallate (0.02%) has been demonstrated to prevent the atherogenic events induced by P. gingivalis, as suggested by reduced mRNA levels of oxidative stress-related mediators found in the aorta of infected mice [80]
Summary
Atherosclerotic cardiovascular diseases (CVDs) continue to represent a major public health problem in developed countries, accounting for one-third of all deaths worldwide [1]. Sci. 2017,stress, 18, 2459 resulting from the imbalance between the production of reactive oxygen species (ROS) and the activity of antioxidant systems, has recently acquired increasing importance. In addition to oxidative stress, another central underlying driver of the atherosclerotic process is the inflammation that promotes the initiation and the evolution of atheroma contributing to the is the inflammation that promotes the initiation and the evolution of atheroma contributing to the precipitation of acute thrombotic complications of unstable plaque [6,7]. We focus on the oxidative mechanisms through which infectious agents may contribute to the early stages of the atherosclerotic process, by promoting endothelial dysfunction, LDL oxidation, and foam cell formation, and to the late stages, by stimulating platelet activation and VSMC migration and proliferation. Potential strategies, targeting pathogen-induced oxidative stress in the prevention of CVDs, are discussed
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