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      Acromegaly, inflammation and cardiovascular disease: a review


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          Acromegaly is characterized by Growth Hormone (GH) and Insulin-like Growth Factor 1 (IGF-1) excess. Uncontrolled acromegaly is associated with a strongly increased risk of cardiovascular disease (CVD), and numerous cardiovascular risk factors remain present after remission. GH and IGF-1 have numerous effects on the immune and cardiovascular system. Since endothelial damage and systemic inflammation are strongly linked to the development of CVD, and have been suggested to be present in both controlled as uncontrolled acromegaly, they may explain the presence of both micro- and macrovascular dysfunction in these patients. In addition, these changes seem to be only partially reversible after remission, as illustrated by the often reported presence of endothelial dysfunction and microvascular damage in controlled acromegaly. Previous studies suggest that insulin resistance, oxidative stress, and endothelial dysfunction are involved in the development of CVD in acromegaly. Not surprisingly, these processes are associated with systemic inflammation and respond to GH/IGF-1 normalizing treatment.

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          Most cited references212

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          Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease.

          Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved.
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            Macrophages in atherosclerosis: a dynamic balance.

            Atherosclerosis is a chronic inflammatory disease that arises from an imbalance in lipid metabolism and a maladaptive immune response driven by the accumulation of cholesterol-laden macrophages in the artery wall. Through the analysis of the progression and regression of atherosclerosis in animal models, there is a growing understanding that the balance of macrophages in the plaque is dynamic and that both macrophage numbers and the inflammatory phenotype influence plaque fate. In this Review, we summarize recently identified pro- and anti-inflammatory pathways that link lipid and inflammation biology with the retention of macrophages in plaques, as well as factors that have the potential to promote their egress from these sites.
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              Western Diet Triggers NLRP3-Dependent Innate Immune Reprogramming

              Long-term epigenetic reprogramming of innate immune cells in response to microbes, also termed “trained immunity,” causes prolonged altered cellular functionality to protect from secondary infections. Here, we investigated whether sterile triggers of inflammation induce trained immunity and thereby influence innate immune responses. Western diet (WD) feeding of Ldlr −/− mice induced systemic inflammation, which was undetectable in serum soon after mice were shifted back to a chow diet (CD). In contrast, myeloid cell responses toward innate stimuli remained broadly augmented. WD-induced transcriptomic and epigenomic reprogramming of myeloid progenitor cells led to increased proliferation and enhanced innate immune responses. Quantitative trait locus (QTL) analysis in human monocytes trained with oxidized low-density lipoprotein (oxLDL) and stimulated with lipopolysaccharide (LPS) suggested inflammasome-mediated trained immunity. Consistently, Nlrp3 −/− / Ldlr −/− mice lacked WD-induced systemic inflammation, myeloid progenitor proliferation, andre-programming. Hence, NLRP3 mediates trained immunity following WD and could thereby mediate the potentially deleterious effects of trained immunity in inflammatory diseases. Systemic inflammation induced by a Western diet is largely blunted by dietary changes, but myeloid cell-induced innate immune responses remain augmented and could potentially contribute to inflammatory disease.

                Author and article information

                Rev Endocr Metab Disord
                Rev Endocr Metab Disord
                Reviews in Endocrine & Metabolic Disorders
                Springer US (New York )
                26 May 2020
                26 May 2020
                : 21
                : 4
                : 547-568
                [1 ]GRID grid.10417.33, ISNI 0000 0004 0444 9382, Department of Internal Medicine, , Radboud University Medical Center Nijmegen, ; Geert Grooteplein Zuid 10, 6525 GA Nijmegen, The Netherlands
                [2 ]GRID grid.10388.32, ISNI 0000 0001 2240 3300, Department for Genomics & Immunoregulation, Life and Medical Sciences Institute (LIMES), , University of Bonn, ; Bonn, Germany
                Author information
                © The Author(s) 2020

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                Funded by: Radboud University Medical Center
                Custom metadata
                © Springer Science+Business Media, LLC, part of Springer Nature 2020

                Endocrinology & Diabetes
                inflammation,insulin-like growth factor-1,cardiovascular disease,acromegaly,growth hormone,cytokines


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