Abstract
Obesity is characterized by the excessive deposition of fat that may interfere with the normal metabolic process of the body. It is a chronic condition associated with various metabolic syndromes, whose prevalence is grossly increasing, and affects both children and adults. Accumulation of excessive macronutrients on the adipose tissues promotes the secretion and release of inflammatory mediators, including interleukin-6 (IL-6), interleukin 1β, tumor necrotic factor-α (TNF-α), leptin, and stimulation of monocyte chemoattractant protein-1 (MCP-1), which subsequently reduce the production of adiponectin thereby initiating a proinflammatory state. During obesity, adipose tissue synthesizes and releases a large number of hormones and cytokines that alter the metabolic processes, with a profound influence on endothelial dysfunction, a situation associated with the formation of atherosclerotic plaque. Endothelial cells respond to inflammation and stimulation of MCP-1, which is described as the activation of adhesion molecules leading to proliferation and transmigration of leukocytes, which facilitates their increase in atherogenic and thromboembolic potentials. Endothelial dysfunction forms the cornerstone of this discussion, as it has been considered as the initiator in the progression of cardiovascular diseases in obesity. Overexpression of proinflammatory cytokines with subsequent reduction of anti-inflammatory markers in obesity, is considered to be the link between obesity-induced inflammation and endothelial dysfunction. Inhibition of inflammatory mechanisms and management and control of obesity can assist in reducing the risks associated with cardiovascular complications.
Highlights
Incidences of obesity are increasing exponentially, and this has contributed effectively to the increasing prevalence of various pathological conditions of obesity-related metabolic disorders
This review summarizes the pathophysiology of the endothelium, and the molecular mechanisms through which adipose tissue secretions in obesity influence endothelial dysfunction
Other related biomarkers include: growth differentiation factor-15 (GDF15), myeloid-related proteins 8/14, pentraxin 3, and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), which were identified as surrogate markers of atherosclerosis associated with cardiovascular diseases during obesity [45,46], while galectin-3 was described as a potential biomarker of vascular remodeling and endothelial dysfunctions attributed to inflammation in obesity [47]
Summary
Incidences of obesity are increasing exponentially, and this has contributed effectively to the increasing prevalence of various pathological conditions of obesity-related metabolic disorders. The balanced release of contracting and endothelial-derived relaxing factors is maintained [6] Alterations in this balance predispose the vascular endothelium towards prothrombotic and proatherogenic states, resulting in platelet activation, leukocyte adherence, vasoconstriction, pro-oxidation, mitogenesis, vascular inflammation, impaired coagulation, atherosclerosis, and thrombosis with subsequent cardiovascular diseases [6]. During obesity, this delicate balance is usually disrupted, promoting the development and further progression to vascular endothelial dysfunction with subsequent damage to some vital organs [5,6]. The mechanisms linking obesity, inflammation, and endothelial dysfunction are discussed
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