Elissavet Kardami – författare

The limitation in number of donor hearts led to the establishment of alternative treatments such as left ventricular assist devices (LVAD), which have been used. Although several reports suggest the native ventricular function recovers after long-term LVAD support - a process called "reverse remodelling" - the underlying biological mechanisms are unclarified. Various molecular pathways of the human myocardium associated with apoptosis, response to stress, or matrix changes are known to be altered under conditions of heart failure and some of them have been shown to be reversible regulated during left ventricular mechanical support. This suggests that the "reverse remodelling" is actually, at least in part, a reverse mechanism. One explanation may be, under mechanical circulatory assist, volume and pressure overload is reduced, and thus ventricular wall stress decreases, leading to improved myocardial blood supply. This may be one explanation for the molecular myocardial changes, and may reflect a possible cause of "reverse remodelling".

Cardiac cell biology has come of age. Recognition of activated or modified signalling molecules by specific antibodies, new selective inhibitors, and fluorescent fusion tags are but a few of the tools used to dissect signalling pathways and cross-talk mechanisms that may eventually allow rational drug design. Understanding the regulation of cardiac hypertrophy in all its complexity remains a fundamental goal of cardiac research. Since the advancement of adenovirally mediated gene transfer, transfection efficiency is no longer a limiting factor in the study of cardiomyocytes. A limiting factor in considering cell transplantion as a strategy to repair the damaged heart is cell availability at the right time. Cardiac gap junctions, intercellular communication channels that allow electrical and metabolic coupling and play an important role in arrhythmogenesis are now understood to be exquisite sensors of cardiac change. The reports in this volume include elegant studies that made use of cutting edge technological advances and many specialized reagents to address these issues.

Cardiac cell biology has come of age. Recognition of activated or modified signaling molecules by specific antibodies, new selective inhibitors, and fluorescent fusion tags are but a few of the tools used to dissect signaling pathways and cross-talk mechanisms that may eventually allow rational drug design. Understanding the regulation of cardiac hypertrophy in all its complexity remains a fundamental goal of cardiac research. Since the advancement of adenovirally mediated gene transfer, transfection efficiency is no longer a limiting factor in the study of cardiomyocytes. A limiting factor in considering cell transplantion as a strategy to repair the damaged heart is cell availability at the right time. Cardiac gap junctions, intercellular communication channels that allow electrical and metabolic coupling and play an important role in arrhythmogenesis are now understood to be exquisite sensors of cardiac change. The reports in this volume incLude elegant studies that made use of cutting edge technological advances and many specialized reagents to address these issues.

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.