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      Adipocytokines in Atherothrombosis: Focus on Platelets and Vascular Smooth Muscle Cells

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          Abstract

          Visceral obesity is a relevant pathological condition closely associated with high risk of atherosclerotic vascular disease including myocardial infarction and stroke. The increased vascular risk is related also to peculiar dysfunction in the endocrine activity of adipose tissue responsible of vascular impairment (including endothelial dysfunction), prothrombotic tendency, and low-grade chronic inflammation. In particular, increased synthesis and release of different cytokines, including interleukins and tumor necrosis factor- α (TNF- α), and adipokines—such as leptin—have been reported as associated with future cardiovascular events. Since vascular cell dysfunction plays a major role in the atherothrombotic complications in central obesity, this paper aims at focusing, in particular, on the relationship between platelets and vascular smooth muscle cells, and the impaired secretory pattern of adipose tissue.

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          The biology of vascular endothelial growth factor.

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            Platelet activation and atherothrombosis.

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              A novel serum protein similar to C1q, produced exclusively in adipocytes.

              We describe a novel 30-kDa secretory protein, Acrp30 (adipocyte complement-related protein of 30 kDa), that is made exclusively in adipocytes and whose mRNA is induced over 100-fold during adipocyte differentiation. Acrp30 is structurally similar to complement factor C1q and to a hibernation-specific protein isolated from the plasma of Siberian chipmunks; it forms large homo-oligomers that undergo a series of post-translational modifications. Like adipsin, secretion of Acrp30 is enhanced by insulin, and Acrp30 is an abundant serum protein. Acrp30 may be a factor that participates in the delicately balanced system of energy homeostasis involving food intake and carbohydrate and lipid catabolism. Our experiments also further corroborate the existence of an insulin-regulated secretory pathway in adipocytes.
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                Author and article information

                Journal
                Mediators Inflamm
                MI
                Mediators of Inflammation
                Hindawi Publishing Corporation
                0962-9351
                1466-1861
                2010
                28 June 2010
                : 2010
                Affiliations
                Department of Clinical and Biological Sciences, Internal Medicine and Metabolic Disease Unit, San Luigi Gonzaga Hospital, San Luigi Gonzaga Faculty of Medicine of the Turin University, Orbassano,10043 Turin, Italy
                Author notes

                Academic Editor: Gema Frühbeck

                Article
                10.1155/2010/174341
                2905911
                20652043
                Copyright © 2010 Giovanni Anfossi et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Review Article

                Immunology

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