Abstract
Heart failure is a major health problem of epidemic proportions. Irrespective of its etiologic origins, a dysfunction of this normally efficient muscular pump is associated with systemic consequences, a progressive downhill clinical course and poor prognosis. Ventricular dysfunction is ultimately accompanied by neurohormonal system activation that accounts for: the congestive heart failure syndrome; an induction of oxi / nitrosative stress; adverse vascular remodeling; and activation of the immune system that contributes to a wasting syndrome known as cardiac cachexia. Circulating effector hormones of the renin-angiotensin-aldosterone system are an integral feature of this neurohormonal activation; they have systemic consequences. Insights into the pathophysiology of heart failure will identify improved methods of prevention, including biomarkers to aid in its detection and identification of risk, and to the development of specific drug targets. Herein we address one aspect of the neurohormonal profile of heart failure, namely that related to aldosteronism. Our focus is directed at the link between aldosteronism and its adverse influence on coronary vasculature structure, a proinflammatory / fibrogenic cardiac phenotype, which is based on an immunostimulatory state that includes activated peripheral blood mononuclear cells.
Keywords: Aldosteronism, cardiac cachexia, Fibrogenic
Current Drug Targets
Title: Aldosteronism in Heart Failure: A Proinflammatory / Fibrogenic Cardiac Phenotype. Search for Biomarkers and Potential Drug Targets
Volume: 4 Issue: 6
Author(s): Karl T. Weber, Ivan C. Gerling, Mohammad F. Kiani, Ramareddy V. Guntaka, Yao Sun, Robert A. Ahokas, Arnold E. Postlethwaite and Kenneth J. Warrington
Affiliation:
Keywords: Aldosteronism, cardiac cachexia, Fibrogenic
Abstract: Heart failure is a major health problem of epidemic proportions. Irrespective of its etiologic origins, a dysfunction of this normally efficient muscular pump is associated with systemic consequences, a progressive downhill clinical course and poor prognosis. Ventricular dysfunction is ultimately accompanied by neurohormonal system activation that accounts for: the congestive heart failure syndrome; an induction of oxi / nitrosative stress; adverse vascular remodeling; and activation of the immune system that contributes to a wasting syndrome known as cardiac cachexia. Circulating effector hormones of the renin-angiotensin-aldosterone system are an integral feature of this neurohormonal activation; they have systemic consequences. Insights into the pathophysiology of heart failure will identify improved methods of prevention, including biomarkers to aid in its detection and identification of risk, and to the development of specific drug targets. Herein we address one aspect of the neurohormonal profile of heart failure, namely that related to aldosteronism. Our focus is directed at the link between aldosteronism and its adverse influence on coronary vasculature structure, a proinflammatory / fibrogenic cardiac phenotype, which is based on an immunostimulatory state that includes activated peripheral blood mononuclear cells.
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Cite this article as:
Weber T. Karl, Gerling C. Ivan, Kiani F. Mohammad, Guntaka V. Ramareddy, Sun Yao, Ahokas A. Robert, Postlethwaite E. Arnold and Warrington J. Kenneth, Aldosteronism in Heart Failure: A Proinflammatory / Fibrogenic Cardiac Phenotype. Search for Biomarkers and Potential Drug Targets, Current Drug Targets 2003; 4 (6) . https://dx.doi.org/10.2174/1389450033490948
DOI https://dx.doi.org/10.2174/1389450033490948 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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