Involvement of Inflammation in Pathogenesis of Arterial and Venous Thromboembolic Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (1 November 2023) | Viewed by 1939

Special Issue Editor


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Guest Editor
Department for Vascular Diseases, University of Ljubljana, Ljubljana, Slovenia
Interests: cardiovascular disease and inflammation; preclinical atherosclerosis: endothelial dysfunction, intima-media thickness

Special Issue Information

Dear Colleagues,

Inflammation represents the basic pathogenetic mechanism of atherosclerosis. Inflammation mediates all stages of the disease, from initiation to the thrombotic complications of atherosclerosis. Raised levels of inflammatory mediators have been reported in subjects with atherosclerosis. Increased risk for CV events is associated with increased levels of cytokines, P-selectin and E-selectin, and acute phase reactants, such as a high sensitivity C-reactive protein and serum amyloid-A represent a risk for cardiovascular events. Elevation of some of these markers predicts the outcomes of patients with acute coronary syndromes and long-term outcomes. Therefore, the role of inflammation in the pathophysiology of arterial thromboembolic events has been elucidated.

However, little is known about the relationship between inflammation and venous thrombosis. Recently, inflammation has been accepted as a possible mechanism through which different risk factors trigger thrombus formation in veins. Patients with idiopathic DVT have long-term increased inflammatory markers. These findings favor the hypothesis that inflammation is a cause and not merely a consequence of acute DVT. Considerable progress in the understanding of the role of inflammation in cardiovascular disease has opened new possibilities for their management. Recently new drugs mediating the direct inhibition of inflammation were developed.

Recent findings indicate that inflammation represents the basic pathogenetic mechanism of arterial atherosclerotic and venous thromboembolic disease. Inflammation represents a common denominator of harmful effects of risk factors, which are involved in venous or arterial disease, particularly atherosclerosis, and deep or superficial venous thrombosis. However, till now the importance of inflammation in the pathogenesis of this disease was neglected and the treatment is mostly based on antithrombotic drugs and the elimination of risk factors. Recently, new drugs with anti-inflammatory effects on vessel walls are developing.

Therefore, the aim of this Special Issue should be: to collect the data on the involvement of inflammation in CV and VTE disease, the relationship between risk factors and inflammation, anti-inflammatory drugs in the prevention and treatment of these diseases.

Prof. Dr. Pavel Poredoš
Guest Editor

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Keywords

  • atherosclerosis
  • inflammation
  • pathogenesis of venous thromboembolic disease
  • anti-inflammatory treatment

Published Papers (1 paper)

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Review

17 pages, 349 KiB  
Review
Hypotheses on Atherogenesis Triggering: Does the Infectious Nature of Atherosclerosis Development Have a Substruction?
by Konstantin A. Lusta, Anastasia V. Poznyak, Vasily N. Sukhorukov, Ilya I. Eremin, Irina I. Nadelyaeva and Alexander N. Orekhov
Cells 2023, 12(5), 707; https://doi.org/10.3390/cells12050707 - 23 Feb 2023
Cited by 3 | Viewed by 1635
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 [...] Read more.
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. Full article
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