Hypotheses on Atherogenesis Triggering: Does the Infectious Nature of Atherosclerosis Development Have a Substruction?

Abstract

Since the end of the 20th century, it has been clear that atherosclerosis is an inflammatory disease. However, the main triggering mechanism of the inflammatory process in the vascular walls is still unclear. To date, many different hypotheses have been put forward to explain the causes of atherogenesis, and all of them are supported by strong evidence. Among the main causes of atherosclerosis, which underlies these hypotheses, the following can be mentioned: lipoprotein modification, oxidative transformation, shear stress, endothelial dysfunction, free radicals’ action, homocysteinemia, diabetes mellitus, and decreased nitric oxide level. One of the latest hypotheses concerns the infectious nature of atherogenesis. The currently available data indicate that pathogen-associated molecular patterns from bacteria or viruses may be an etiological factor in atherosclerosis. This paper is devoted to the analysis of existing hypotheses for atherogenesis triggering, and special attention is paid to the contribution of bacterial and viral infections to the pathogenesis of atherosclerosis and cardiovascular disease.

Association of coronary atherosclerosis with stutzerimonas stutzeri strains (HaSa 1, 2, 3, and 4) of biofilmforming bacteria

“…These diseases are linked to chronic infection in humans, as research has shown that these gatherings of biofilms release many virulence factors including toxins and proteases (13,14) thus damaging host tissues. Biofilm infection also poses additional risks to the host due to its low exposure to antibiotics and its ability to compete with the host for oxygen and nutrients (15,16). One of the most important activities of biofilms is the response Dispersion which releases bacteria from within the biofilm by decomposition of the biofilm matrix (17).…”

Encompassing view of spatial and single-cell RNA-seq renews the role of the microvasculature in human atherosclerosis

“…The accumulation of these substances results in a complex pathophysiology with various cellular interactions and modulations involved that can result in vascular occlusion and/or plaque rupture or erosion that clinically manifests as myocardial infarction and stroke 3 . Importantly, there is accumulating evidence supporting a high degree of diversity of mechanisms underlying atherosclerotic disease and related thrombotic events 4,5 . Recent single-cell sequencing studies have revealed cellular resolution insights into atherosclerotic tissue in mice and humans, shedding light on cellular heterogeneity, cellular plasticity, and the contribution of different cell types to atherogenesis 6 .…”