Endothelial Dysfunction in Chronic Inflammatory Diseases

Abstract

Chronic inflammatory diseases are associated with accelerated atherosclerosis and increased risk of cardiovascular diseases (CVD). As the pathogenesis of atherosclerosis is increasingly recognized as an inflammatory process, similarities between atherosclerosis and systemic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel diseases, lupus, psoriasis, spondyloarthritis and others have become a topic of interest. Endothelial dysfunction represents a key step in the initiation and maintenance of atherosclerosis and may serve as a marker for future risk of cardiovascular events. Patients with chronic inflammatory diseases manifest endothelial dysfunction, often early in the course of the disease. Therefore, mechanisms linking systemic inflammatory diseases and atherosclerosis may be best understood at the level of the endothelium. Multiple factors, including circulating inflammatory cytokines, TNF-α (tumor necrosis factor-α), reactive oxygen species, oxidized LDL (low density lipoprotein), autoantibodies and traditional risk factors directly and indirectly activate endothelial cells, leading to impaired vascular relaxation, increased leukocyte adhesion, increased endothelial permeability and generation of a pro-thrombotic state. Pharmacologic agents directed against TNF-α-mediated inflammation may decrease the risk of endothelial dysfunction and cardiovascular disease in these patients. Understanding the precise mechanisms driving endothelial dysfunction in patients with systemic inflammatory diseases may help elucidate the pathogenesis of atherosclerosis in the general population.

Increased risk of migraine in patients with psoriasis: A Danish nationwide cohort study

“…Indeed, recent research has focused on the link between pain and inflammation, and increased tumor necrosis factor-alfa levels, activation of mitogen-activated protein kinases, and endothelial dysfunction are among inflammatory mechanisms that appear to be shared by psoriasis and migraine. [6][7][8][9][10][11][12]27 Along this line, tumor necrosis factor-alfa inhibition may inhibit pain signaling in experimental arthritis and ameliorate endothelial dysfunction in those with psoriasis and psoriatic arthritis, suggesting the potential for targeted anti-inflammatory pharmacologic therapy in the treatment of migraine. [28][29][30] Only very few studies have to our knowledge reported on the association between psoriasis and migraine.…”

Frailty and sarcopenia as the basis for the phenotypic manifestation of chronic diseases in older adults

“…Arterial stiffness is linked to endothelial dysfunction as suggested by the impairment of endothelial vasodilation that always precedes arterial stiffness (Scuteri et al, 2008). Endothelial dysfunction represents a key step in the initiation and maintenance of atherosclerosis and is an independent predictor of cardiovascular events (Steyers and Miller, 2014). Endothelial dysfunction, manifested by a reduction of the endothelium-dependent vasodilation, is associated with the aging process in both the micro and the macrovasculature of animal models (Dal-Ros et al, 2012;Gano et al, 2014;Lakatta and Levy, 2003) and humans Toda, 2012;Walker and Hakkinen, 2014).…”

Macrophages Aggravate Hypoxia-Induced Cardiac Microvascular Endothelial Cell Injury via Peroxynitrite: Protection by Tongxinluo

“…Since the endothelial cell layer constitutes the primary internal barrier of blood vessels, microvascular endothelial dysfunction is believed to be the initiating process and pathological basis of cardiovascular disease (Ding et al, 2014;Steyers & Miller, 2014;Tousoulis et al, 2014;Hald et al, 2014). Although activated macrophages aggravate endothelial cell injury in hypoxia, the mediator has not been defined (Weldy et al, 2011;Mei et al, 2014).…”

“…Atherosclerosis and the subsequent vessel destruction are the primary cause of ischemic diseases, such as stroke and coronary heart disease (Schiano et al, 2014;Tano & Gollasch, 2014). Microvascular endothelial dysfunction is believed to be the initiating process and pathological basis of cardiovascular disease (Ding et al, 2014;Steyers & Miller, 2014;Tousoulis et al, 2014).…”