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      Association of Serum Chemerin Levels with Coronary Artery Disease: Pathogenesis and Clinical Research

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          Abstract

          Recent studies have revealed that chemerin plays an essential role in the development of cardiovascular diseases. Autopsy studies found a strong correlation between the secretion of chemerin in peripheral tissues and aortic and coronary atherosclerosis. Plasma chemerin is a marker of systemic inflammation and is associated with metabolic syndrome. Chemerin plays a vital role in vascular inflammation and atherogenesis. Plasma chemerin levels are increased in patients with dilated cardiomyopathy, and chemerin is associated with left ventricular dysfunction. In this review, we focus on chemerin expression, chemerin processing, its biological function, and its role in the diagnosis of cardiovascular diseases.

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          Most cited references 33

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          Inflammation, immunity, and hypertensive end-organ damage.

          For >50 years, it has been recognized that immunity contributes to hypertension. Recent data have defined an important role of T cells and various T cell-derived cytokines in several models of experimental hypertension. These studies have shown that stimuli like angiotensin II, deoxycorticosterone acetate-salt, and excessive catecholamines lead to formation of effector like T cells that infiltrate the kidney and perivascular regions of both large arteries and arterioles. There is also accumulation of monocyte/macrophages in these regions. Cytokines released from these cells, including interleukin-17, interferon-γ, tumor necrosis factorα, and interleukin-6 promote both renal and vascular dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resistance. The renal effects of these cytokines remain to be fully defined, but include enhanced formation of angiotensinogen, increased sodium reabsorption, and increased renal fibrosis. Recent experiments have defined a link between oxidative stress and immune activation in hypertension. These have shown that hypertension is associated with formation of reactive oxygen species in dendritic cells that lead to formation of gamma ketoaldehydes, or isoketals. These rapidly adduct to protein lysines and are presented by dendritic cells as neoantigens that activate T cells and promote hypertension. Thus, cells of both the innate and adaptive immune system contribute to end-organ damage and dysfunction in hypertension. Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke.
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            Chronic Heart Failure and Inflammation: What Do We Really Know?

            As a greater proportion of patients survive their initial cardiac insult, medical systems worldwide are being faced with an ever-growing need to understand the mechanisms behind the pathogenesis of chronic heart failure (HF). There is a wealth of information about the role of inflammatory cells and pathways during acute injury and the reparative processes that are subsequently activated. We discuss the different causes that lead to chronic HF development and how the sum of initial inflammatory and reparative responses only sets the trajectory for disease progression. Unfortunately, comparatively little is known about the contribution of the immune system once the trajectory has been set, and chronic HF has been established-which clinically represents the majority of patients. It is known that chronic HF is associated with circulating inflammatory cytokines that can predict clinical outcomes, yet the causative role inflammation plays in disease progression is not well defined, and the majority of clinical trials that target aspects of inflammation in patients with chronic HF have largely been negative. This review will present what is currently known about inflammation in chronic HF in both humans and animal models as a means to highlight the gap in our knowledge base that requires further examination.
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              Identification of chemerin receptor (ChemR23) in human endothelial cells: chemerin-induced endothelial angiogenesis.

              Chemerin acting via its distinct G protein-coupled receptor CMKLR1 (ChemR23), is a novel adipokine, circulating levels of which are raised in inflammatory states. Chemerin shows strong correlation with various facets of the metabolic syndrome; these states are associated with an increased incidence of cardiovascular disease (CVD) and dysregulated angiogenesis. We therefore, investigated the regulation of ChemR23 by pro-inflammatory cytokines and assessed the angiogenic potential of chemerin in human endothelial cells (EC). We have demonstrated the novel presence of ChemR23 in human ECs and its significant up-regulation (P<0.001) by pro-inflammatory cytokines, TNF-alpha, IL-1beta and IL-6. More importantly, chemerin was potently angiogenic, as assessed by conducting functional in-vitro angiogenic assays; chemerin also dose-dependently induced gelatinolytic (MMP-2 & MMP-9) activity of ECs (P<0.001). Furthermore, chemerin dose-dependently activated PI3K/Akt and MAPKs pathways (P<0.01), key angiogenic and cell survival cascades. Our data provide the first evidence of chemerin-induced endothelial angiogenesis and MMP production and activity. Copyright 2009 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                CVIA
                Cardiovascular Innovations and Applications
                CVIA
                Compuscript (Ireland )
                2009-8782
                2009-8618
                July 2020
                July 2020
                : 4
                : 4
                : 251-256
                Affiliations
                1Department of Cardiology, Adiyaman Education and Research Hospital, Adiyaman, Turkey
                2Department of Cardiology, Faculty of Medicine, Recep Tayyip Erdogan University, Rize, Turkey
                Author notes
                Correspondence: Lutfu Askin, MD, Associate Professor, Department of Cardiology, Adiyaman Education and Research Hospital, 2230-Adiyaman, Turkey, Tel.: +90-531-5203486, Fax: +90-4161015, E-mail: lutfuaskin23@ 123456gmail.com
                Article
                cvia20190572
                10.15212/CVIA.2019.0572
                Copyright © 2020 Cardiovascular Innovations and Applications

                This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 Unported License (CC BY-NC 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. See https://creativecommons.org/licenses/by-nc/4.0/.

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