Author: Wirt Anderson HinesPublisher:
ISBN:
Category : Heart
Languages : en
Pages : 200
Book Description
Signal Transduction Mechanisms Regulating Cardiac Myocyte Hypertrophy and Gene Expression
Author: Wirt Anderson HinesPublisher:
ISBN:
Category : Heart
Languages : en
Pages : 200
Book Description
Signal Transduction and Cardiac Hypertrophy
Author: Naranjan S. DhallaPublisher: Springer Science & Business Media
ISBN: 1461503477
Category : Medical
Languages : en
Pages : 778
Book Description
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.
Signaling in the Heart
Author: José Marín-GarcíaPublisher: Springer Science & Business Media
ISBN: 1441994610
Category : Medical
Languages : en
Pages : 511
Book Description
Signal transduction pathways are at the core of most biological processes and are critical regulators of heart physiology and pathophysiology. The heart is both a transmitter and dynamic receptor of a variety of intracellular and extracellular stimuli, playing a critical role of an integrator of diverse signaling mechanisms. Alterations in signaling pathways are contributing factors in the development and progression of a broad spectrum of diseases, ranging from dysrhythmias and atherosclerosis to hypertension and the metabolic syndrome. Targeting specific components of these signaling pathways has been shown to be effective in preclinical studies with significant therapeutic impact. This book brings together current knowledge in cardiovascular cell signal transduction mechanisms, advances in novel therapeutic approaches to improve cardiac function, and discussion of future directions. Presented from a post-genomic perspective, this exciting book introduces important new ideas in cardiovascular systems biology. It is an invaluable reference for cardiology researchers and practitioners.
Signal Transduction Mechanisms and Nuclear Effectors in Gene Expression During Hypertrophy of Cardiac Myocytes
Author: Sampsa PikkarainenPublisher:
ISBN: 9789514270376
Category :
Languages : en
Pages : 100
Book Description
Regulation of Myocardial Growth and Apoptosis by Stress Kinase Signal Transduction Pathways in Neonatal Cardiac Myocytes
Author: Dietmar K. ZechnerPublisher:
ISBN:
Category : Cellular signal transduction
Languages : en
Pages : 516
Book Description
During the clinical pathology of cardiac hypertrophy, the expression pattern of genes and morphological features of ventricular myocytes change. As cardiac myocytes re-express embryonic genes such as the hormone, atrial natriuretic factor, or $\alpha$-skeletal actin their cell size increases and sarcomeric organization is induced. At the late stage of cardiac hypertrophy, apoptosis can be observed contributing to the deterioration of the heart. Utilizing neonatal ventricular myocytes as a model system, the potential involvement of the JNK and p38 stress kinase signal transduction pathways in the induction of hypertrophic features and apoptosis was tested. To specifically activate or inhibit JNK or p38 signaling, plasmids expressing constitutively-active or dominant-negative kinases, known to be part of either pathway, were transfected into ventricular myocytes. Moreover the SB 203580 compound was utilized to inhibit p38 specifically. Activation of the p38 signal transduction pathway by cotransfection of MKK6 or stimulation by phenylephrine induces atrial natriuretic factor, as well as alpha-skeletal actin, promoter activity, and increases cell size and sarcomeric organization, while inhibiting apoptosis. JNK signaling, can cooperate with p38 signaling pathways in the induction of atrial natriuretic factor promoter activity. However, constitutively active MEKK1, which can activate ERK, JNK and p38 in cardiac myocytes, can also induce apoptosis in ventricular myocytes. This study suggests the involvement of stress kinase signal transduction pathways in the regulation of hypertrophy and apoptosis in neonatal ventricular myocytes.
Biochemistry of Signal Transduction in Myocardium
Author: Jos M.J. LamersPublisher: Springer Science & Business Media
ISBN: 1461312752
Category : Science
Languages : en
Pages : 263
Book Description
The chapters in this volume are the Proceedings of the Satellite Symposium of the XVIth World Congress of the International Society for Heart Research on `Signal Transduction in Normal and Diseased Myocardium' which was held in Rotterdam at the Faculty of Medicine & Health Sciences of the Erasmus University, June 30 and July 1, 1995. Diverse and distinct auto-, para-, and endocrine stimuli arriving at the surface of endothelium, smooth muscle cells, cardiomyocytes and fibroblasts within the myocardium, engage cell type-specific receptors, which lead to transmission of signals across the cell plasma membrane and result in the production and activation of second messengers. The most common mechanism by which these second messengers function is via direct or indirect activation of specific protein kinases. The current challenge for scientists is to identify the specific substrates (e.g. metabolic enzymes, Ca2+-regulating proteins, transcription and mitotic factors) for the many protein kinases, to elucidate the biological significance of the cell type-specific expression heterogeneity of signalling proteins (e.g. membrane receptors, isoenzymes of protein kinase C, G-proteins) and to unravel the cross-talk interaction between the signalling systems (e.g. phospholipase C with adenylate cyclase and phospholipase C with phospholipase D). The multiplicity of receptor types, G-proteins, effector proteins, second messengers and protein kinases, their substrate proteins and the `cross-talk' interactions in the myocardium raises fundamental questions about the mechanisms that ensure the precision and timing of the myocardial responses to hormonal and pharmacological stimuli. This book provides an up-to-date source of information for all scientists and clinicians interested in the mechanisms by which external signals are transmitted to the interior and regulation of a variety of physiological, pathological and pharmacological responses.
Cardiac Mechanotransduction
Author: Matti WeckströmPublisher: Springer Science & Business Media
ISBN: 0387488685
Category : Medical
Languages : en
Pages : 158
Book Description
This book presents a multidisciplinary approach to cardiac mechanotransduction. The chapters depict the many faces of the topic, from membrane and ion channel level to mechanics, biochemical signaling and regulation via hormone systems. Cardiac Mechanotransduction is of interest to basic life sciences, like physiology, biochemistry and pharmacology, but also to clinicians working with heart-related problems, such as cardiologists and internists.
Signal Transduction in the Cardiovascular System in Health and Disease
Author: Ashok K. SrivastavaPublisher: Springer Science & Business Media
ISBN: 0387095527
Category : Medical
Languages : en
Pages : 426
Book Description
Signal Transduction in Cardiovascular System Health and Disease highlights the major 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 title is volume 3 in the new Springer series, Advances in Biochemistry in Health and Disease.
Mechanoresponsive Mechanisms In Hypertrophic Cardiac Remodeling
Author: Todd Haswell KimballPublisher:
ISBN:
Category :
Languages : en
Pages : 0
Book Description
All cells of the body are under some form of mechanical load and these forces are part of the factors defining cell type specificity. The mechanical environment influences cellular behavior and is the basis of mechanobiology. The forces acting on cells must be met with a cellular response, as the input signals are transduced to molecular mechanisms that drive gene regulation. In the heart, the distinct roles of cardiomyocytes and fibroblasts, as fibroblasts enforce tissue stiffness homeostasis through extracellular matrix maintenance and cardiomyocyte contraction-relaxation cycles work against this stiffness with every heartbeat, enable each to respond to cardiac stressors through differential gene expression, changing their cellular physical phenotype. At the cellular level, cardiac hypertrophy is a growth of the cardiomyocyte (without proliferation) and increased interstitial fibrosis, and these phenotypes are the result of changes to gene expression. While the gene expression program induced by cardiac hypertrophy is well documented, this dissertation unravels mechanosensitive mechanisms activated by changes to the myocardial environment and cellular forces driving dysfunctional gene regulation perpetuating cardiac disease. Gene translation ends in the nucleus; however, it does not always start there. We viewed gene expression as an end point, being influenced by a number of factors outside the nucleus, including metabolism, nucleoskeletal, cytoskeletal, sarcomere organization, sarcolemmal signal transduction pathways, and the tissue environment. In examining transcriptional influence outside the nucleus, we first summarize the bidirectional effect of metabolic and gene regulation dysfunction in heart disease, as metabolic substrates and intermediates impact cardiac epigenetics and chromatin stores information. We report our findings from our pressure overload induced cardiac hypertrophy studies, demonstrating cardiomyocyte cellular remodeling influences nucleoskeletal ultrastructure through the expression of the structural and chromatin binding protein Lamin A/C. We phenotypically characterize an [alpha]1-adrenergic model of cardiac hypertrophy and investigate cell specific mechanism driving tissue remodeling and cellular mechanosensitive pathways underlying pathological stress. Through these studies, we explore the cardiac stressors that remodel the heart tissue during hypertrophy and the cellular mechanisms altering the cellular phenotype through gene regulation.
The Hypertrophied Heart
Author: Nobuakira TakedaPublisher: Springer Science & Business Media
ISBN: 1461544238
Category : Medical
Languages : en
Pages : 490
Book Description
Whenever the heart is challenged with an increased work load for a prolonged period, it responds by increasing its muscle mass--a phenomenon known as cardiac hypertrophy. Although cardiac hypertrophy is commonly seen under physiological conditions such as development and exercise, a wide variety of pathological situa tions such as hypertension (pressure overload), valvular defects (volume overload), myocardial infarction (muscle loss), and cardiomyopathy (muscle disease) are also known to result in cardiac hypertrophy. Various hormones such as catecholamines, thyroid hormones, angiotensin II, endothelin, and growth factors have also been shown to induce cardiac hypertrophy. Although the exact mechanisms underlying or pathological forrns of cardiac hypertrophy are poorly under the physiological stood, an increase in the intraventricular pressure is believed to represent the major stimulus for the development of cardiac hypertrophy. In this regard, stretching of the cardiac muscle has been shown to induce the hypertrophic response, but the role of metabolic influences in this process cannot be ruled out. Furthermore, different hormones and other interventions in the absence of stretch have been observed to stimulate protein synthesis in both isolated cardiomyocyte and vascular myocyte preparations. Nonetheless, it is becoming dear that receptor as well as phospholipid linked signal transduction pathways are activated in some specific manner depend ing upon the initial hypertrophic stimulus, and these then result in an increase in the size and mass of cardiomyocytes.