Abstract
Throughout the years, a growing number of studies have provided evidence that oxidative stress and inflammation may be involved in the pathogenesis of infectious agent-related cardiovascular diseases. Amongst the numerous respiratory pathogens, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus responsible for the global ongoing pandemic, and Chlamydia pneumoniae, a widely known intracellular obligate bacteria, seem to have an essential role in promoting reactive oxygen species and cytokine production. The present review highlights the common oxidative and inflammatory molecular pathways underlying the cardiovascular diseases associated with SARS-CoV-2 or C. pneumoniae infections. The main therapeutic and preventive approaches using natural antioxidant compounds will be also discussed.
Highlights
Oxidative stress and inflammation have been identified as relevant pathophysiological pathways in the development of cardiovascular diseases (CVDs), with increasing evidence showing their complex interplay in all the stages leading to CVDs, from endothelial dysfunction to thrombosis [1,2]
In addition to the encouraging effects of antioxidants in in vitro studies, a metaanalysis of randomized clinical trials has shown that there is no evidence to support the use of vitamins for the prevention of CVDs [101], a recent clinical trial has shown that lycopene, a member of the carotenoid family with antioxidant properties, decreased the levels of oxidized low-density lipoprotein (LDL) and tissue damage, as well as the levels of C. pneumoniae IgG, in patients with coronary vascular disease [102]
Despite the different natures of SARS-CoV-2 and C. pneumoniae, the first a novel respiratory virus and the latter an intracellular obligate bacterium, both depend on the host cell for their replication and possess high tropism for lung tissue, the primary site of infection and starting point for the dissemination for either of these pathogens in the host organism
Summary
Oxidative stress and inflammation have been identified as relevant pathophysiological pathways in the development of cardiovascular diseases (CVDs), with increasing evidence showing their complex interplay in all the stages leading to CVDs, from endothelial dysfunction to thrombosis [1,2]. It has been recently demonstrated that SARS-CoV-2 is able to infect the endothelium, leading to endothelial dysfunction that can result in predisposition to thrombosis in all arterial beds of the microvasculature, including the pulmonary and coronary circulation as well as the peripheral veins and arteries of the cerebral circulation, potentially causing strokes [19,20]. This is further confirmed by the high D-dimer levels found in 20–40% of critically ill patients as an attempt to dissolve thrombotic clots [21]. Cellular and Molecular Pathways Related to Oxidative Stress and Inflammation in SARS-CoV-2 and C. pneumoniae Infections
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