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NotificationsNotify me of updates to Glucocorticoid Receptor Signaling and its Potential Convergence with Toll-Like Receptor (TLR)-4 and Receptor for Advanced Glycation End-Products (RAGE) Signaling Pathways in Cardiovascular Disease pp. 1-34
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Glucocorticoid Receptor Signaling and its Potential Convergence with Toll-Like Receptor (TLR)-4 and Receptor for Advanced Glycation End-Products (RAGE) Signaling Pathways in Cardiovascular Disease pp. 1-34 $0.00
Authors:  (Vasileios Salpeas, James N. Tsoporis, Shehla Izhar, Thomas G. Parker, Ekaterini S. Bei, Paraskevi Moutsatsou, Ioannis K. Rizos, 2nd Academic Department of Cardiology, Attikon University Hospital, University of Athens Medical School, Athen, Greece, and others)
Abstract:
Glucocorticoid administration has been considered for the reduction of atherosclerosis and restenosis following percutaneous coronary intervention. Excess of glucocorticoids (GCs), due to either chronic exogenous treatment or to endogenous hypersecretion of cortisol (such as depression, systemic inflammation and Cushing disease) has been associated with increased cardiovascular risk. The GC receptor is the cornerstone molecule mediating GCs‘ cellular effects. Myocyte sensitivity to GCs depends on intracellular, pre-receptor metabolism of active cortisol to inactive cortisone by the enzyme 11β-hydroxy steroid dehydrogenase. The molecular basis of GC-induced cardiovascular effects such as atherosclerosis and hypertension remain elusive. Toll-like receptors (TLRs) represent the first line of host defense against microbial infection and play a significant role in both innate and adaptive immunity by recognition of exogenous pathogen-associated molecular patterns and endogenous ligands. The TLR and GR signaling pathways interact and modulate the inflammatory response. Innate immune and inflammatory pathways have been implicated in cardiac dysfunction after global myocardial ischemia. There are 10 TLRs identified to date and they bind to a variety of pathogenic agents such as lipopeptide (TLR2) and lipopolysaccharide (TLR4) by molecular pattern recognition. TLR4 is expressed in myocardial cells and increased expression of this receptor is observed in cardiac myocytes from human and animal models of ischemic cardiac injury. Stimulation of TLRs leads to the activation of various downstream transcription factors in particular nuclear factor (NF)-B and the production of inflammatory cytokines in myocardial cells. These cytokines in turn activate TLRs in a positive feedback mechanism that sustains inflammation thereby contributing to disease progression. S100B, a member of the S100 family of calcium-binding proteins is induced by adrenergic stimulation in myocardial cells following ischemic cardiac injury and depending on the concentration achieved, via receptor for advanced ligation endproducts (RAGE) ligation, results in activation of NF-B and trophic or apoptotic cell responses. Preliminary data from hypoxic myocardial cells demonstrate a possible association between TLR4 and S100B. The common signaling pathway involves the activation of NF-B leading to GC receptor activation and transrepression of target genes. In this chapter we provide a comprehensive review of GC receptor signaling and its convergence with TLR4- and RAGE-S100B dependent signaling pathways as it relates to inflammation and the progression of cardiovascular disease. 


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Glucocorticoid Receptor Signaling and its Potential Convergence with Toll-Like Receptor (TLR)-4 and Receptor for Advanced Glycation End-Products (RAGE) Signaling Pathways in Cardiovascular Disease pp. 1-34