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      Increased plasma soluble endoglin levels as an indicator of cardiovascular alterations in hypertensive and diabetic patients

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          Abstract

          Background

          Endoglin is involved in the regulation of endothelial function, but there are no studies concerning its relation with hypertension- and diabetes-associated pathologies. Thus, we studied the relationship between plasma levels of soluble endoglin and cardiovascular alterations associated with hypertension and diabetes.

          Methods

          We analyzed 288 patients: 64 with type 2 diabetes, 159 with hypertension and 65 healthy patients. We assessed the relationship of soluble endoglin plasma levels measured by enzyme-linked immunosorbent assay with basal glycemia, glycosylated hemoglobin, blood pressure, endothelial dysfunction (assessed by pressure wave velocity), hypertensive retinopathy (by Keith-Wagener classification), left ventricular hypertrophy (by Cornell and Sokolow indexes), cardiovascular risk and target organ (heart, vascular, kidney) damage.

          Results

          There are significant correlations between endoglin and glycemia, systolic blood pressure, pulse pressure, pressure wave velocity and electrocardiographically assessed left ventricular hypertrophy. Endoglin levels were significantly higher in patients with diabetes who had nondipper and extreme dipper circadian blood pressure patterns than in dipper circadian patterns, in patients with hypertension and diabetes who had riser pattern than in the other patients, and in patients with diabetes but not hypertension who had extreme dipper pattern than in dipper, nondipper and riser groups. There was also a significant correlation between plasma-soluble endoglin and lower levels of systolic night-day ratio. Higher endoglin levels were found in patients with diabetes who had retinopathy, in patients with diabetes who had a high probability of 10-year cardiovascular risk, and in patients with diabetes and hypertension who had three or more damaged target organs (heart, vessels, kidney) than in those with no organs affected.

          Conclusions

          This study shows that endoglin is an indicator of hypertension- and diabetes-associated vascular pathologies as endothelial dysfunction and cardiovascular damage.

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          Most cited references38

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          Molecular understanding of hyperglycemia's adverse effects for diabetic complications.

          Diabetic complications are the major cause of morbidity and mortality in persons with diabetes. Chronic hyperglycemia is a major initiator of diabetic microvascular complications (eg, retinopathy, neuropathy, nephropathy). Glucose processing uses a variety of diverse metabolic pathways; hence, chronic hyperglycemia can induce multiple cellular changes leading to complications. Several predominant well-researched theories have been proposed to explain how hyperglycemia can produce the neural and vascular derangements that are hallmarks of diabetes. These theories can be separated into those that emphasize the toxic effects of hyperglycemia and its pathophysiological derivatives (such as oxidants, hyperosmolarity, or glycation products) on tissues directly and those that ascribe pathophysiological importance to a sustained alteration in cell signaling pathways (such as changes in phospholipids or kinases) induced by the products of glucose metabolism. This article summarizes these theories and the potential therapeutic interventions that may prevent diabetic complications in the presence of hyperglycemia, control of which is often difficult with current therapeutic options.
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            Practice guidelines of the European Society of Hypertension for clinic, ambulatory and self blood pressure measurement.

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              Defective angiogenesis in mice lacking endoglin.

              Endoglin is a transforming growth factor-beta (TGF-beta) binding protein expressed on the surface of endothelial cells. Loss-of-function mutations in the human endoglin gene ENG cause hereditary hemorrhagic telangiectasia (HHT1), a disease characterized by vascular malformations. Here it is shown that by gestational day 11.5, mice lacking endoglin die from defective vascular development. However, in contrast to mice lacking TGF-beta, vasculogenesis was unaffected. Loss of endoglin caused poor vascular smooth muscle development and arrested endothelial remodeling. These results demonstrate that endoglin is essential for angiogenesis and suggest a pathogenic mechanism for HHT1.
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                Author and article information

                Journal
                BMC Med
                BMC Medicine
                BioMed Central
                1741-7015
                2010
                20 December 2010
                : 8
                : 86
                Affiliations
                [1 ]Unidad de Fisiopatología Renal y Cardiovascular, Instituto Reina Sofía de Investigación Nefrológica, Universidad de Salamanca, Salamanca, Spain
                [2 ]Unidad de Investigación, Centro de Salud La Alamedilla, SACYL, Salamanca, Spain
                [3 ]Servicio de Medicina Interna, Hospital Universitario de Salamanca, Salamanca, Spain
                [4 ]Instituto de Estudios de Ciencias de la Salud de Castilla y León (IECSCYL), Unidad de Investigación, Hospital Universitario de Salamanca, Paseo San Vicente 58-182, 37007 Salamanca, Spain
                Article
                1741-7015-8-86
                10.1186/1741-7015-8-86
                3012013
                21171985
                c89ec12c-3e94-4c49-89fc-d6df9a7d2e5f
                Copyright ©2010 Blázquez-Medela et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<url>http://creativecommons.org/licenses/by/2.0</url>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 21 September 2010
                : 20 December 2010
                Categories
                Research Article

                Medicine
                Medicine

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