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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.
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."
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