Signal Transduction in the Cardiovascular System in Health and Disease

Abstract

except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. Cover illustration:Printed on acid-free paper 9 8 7 6 5 4 3 2 1 springer.com PrefaceIn recent years, there has been a surge of interest in studies related to the role of a variety of signaling pathways in the control of cardiovascular physiology. Evidence has also accumulated to suggest that an aberration in the signal transduction pathways contributes to the pathophysiology of cardiovascular disease. Several components of the signaling pathways have been identified as potential targets for the development of new therapies of cardiovascular disease. Therefore, this volume has been compiled to highlight the contributions of different signaling systems in modulating normal cardiovascular functions and how a perturbation in these signaling events leads to abnormal cell functions and cardiovascular disorders. This volume has been divided into five sections dealing with five key signaling pathways regulating different aspects of cardiovascular physiology. The first section describes the role of G-protein-coupled receptor (GPCR) signaling in cardiovascular functions. In this section, Anand-Srivastava has elegantly summarized studies showing that the expression levels of various G-proteins as well as responsiveness of adenylyl cyclase systems to various stimuli such as β-adrenergic receptor (βAR) agonist and vasoactive peptides are defective in various models of hypertension, congestive heart failure (CHF), cardiac hypertrophy, and other diseases. Dent et al. have highlighted studies showing how the alterations in different components of the βAR signaling system contribute to CHF and suggest that βAR blockade could be used as a strategy to treat CHF. Continuing on the same theme, Vacek et al. have reviewed the pathophysiological mechanisms involved in CHF and sudden cardiac death, with an emphasis on the role of homocysteine-induced cross talk between NMDA receptor and GPCRs, while Moolman et al. have elaborated on the contributions of adenosine, cAMP/PKA system as well as p 38mapk in eliciting a cardioprotective response during early preconditioning. This section also has two elegant articles on the role of angiotensin II in cardiovascular pathophysiology: Engberding and Grindling and Schaffer and Mozaffari have provided indepth accounts of various signaling pathways induced by angiotensin II and how the dysregulation of this pathway contributes to heightened growth, proliferation, hypertrophy, and cell survival death responses associated with various cardiovascular abnormalities. v vi PrefaceThe second section foc...