Signal Transduction and Cardiac Hypertrophy

World Heart Congress 2001; Dhalla, Naranjan S. (EDT); Hryshko, Larry V. (EDT); Kardami, Elissavet (EDT); Singal, Pawan K. (EDT); Dhalla, Naranjan S.

ISBN 10: 140207218X / ISBN 13: 9781402072185

Published by Springer, 2003

About this Item

Unread book in perfect condition.

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Bibliographic Details

• Title: Signal Transduction and Cardiac Hypertrophy
• Publisher: Springer
• Publication Date: 2003
• Language: English
• ISBN 10: 140207218X
• ISBN 13: 9781402072185
• Binding: Hardcover
• Condition: As New

About this title

Synopsis

Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand­ ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for their dissection. Moreover, this infor­ mation is beginning to provide tangible targets towards manipulating cardiac func­ tion in the setting of cardiovascular disease. The mechanisms and factors that regulate cardiac cell growth are of particular interest as both adaptive and maladaptive responses can occur during cardiac hypertrophy. Cardiac hypertrophy describes the increase in individual cardiac myocyte size that is accomplished through the series and/or parallel addition of sarcomeres. The ability of cardiac muscle to increase in size through hyperplasia becomes highly restricted or negligible shortly after birth. Consequently, the increase in heart size associated with development and growth of an individual occurs through hypertrophy. In response to a chronic increase in workload, cardiac muscle cells can dramatically increase in size to face their increasing contractile demands. While this plasticity is clearly a ben­ eficial response under many conditions, it can be highly deleterious and inappropri­ ate under others. For example, cardiac hypertrophy associated with endurance exercise clearly enhances athletic performance. In contrast, the hypertrophy associated with chronic hypertension, stenotic or regurgitant heart valves, or following a myocardial infarction often continues far beyond the period where this adaptive response is ben­ eficial.