1 edition of symposium, from increased energy metabolism to cardiac hypertrophy and failure found in the catalog.
symposium, from increased energy metabolism to cardiac hypertrophy and failure
|Other titles||From increased energy metabolism to cardiac hypertrophy and failure., American journal of cardiology. Vol. 83, no. 12A (Supplement)|
|Statement||guest editors, Heinrich Taegtmeyer, Guenther J. Dietze.|
|The Physical Object|
|Pagination||98 p. :|
|Number of Pages||98|
A year-old female has increased pulmonary pressure resulting in right heart failure. The nurse should monitor for a possible complication because a potential cause for her heart . Keywords: Cardiac energy metabolism, diabetes, fatty acid utilization, mitochondrial uncoupling Introduction It is well recognized that patients with diabetes mel-litus have an increased risk of cardiac disease that is independent of the presence of secondary risk factors such as coronary artery disease [1,2]. A large body of.
Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic Cited by: In left ventricular hypertrophy and heart failure, these processes become disturbed, leading as will be discussed to impaired cardiac energetic status and to further impairment of cardiac function. These metabolic disturbances form a potential target for by:
The failing heart is unable to maintain its energetic reserve. Alterations in myocardial high‐energy phosphates were identified in animal models and human hearts with LV hypertrophy or heart failure. A decrease in PCr/ATP ratio is consistently reported in failing human heart and experimental heart failure, even at moderate by: This volume of Advances in Myocardiology is derived from a part of the proceedings of the 10th Congress of the International Society for Heart Research, which was held in Moscow on September , This book contains selected papers which have been arranged in two sections, Cardiac Hypertrophy, Adaptation, and Pathophysiology and Cardiac Hypoxia, Is chemia, and Infarction. The first.
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Cardiac Energy Metabolism in Health and Disease describes the research advances that have been made in understanding what controls cardiac energy metabolism at molecular, transcriptional, and physiological levels. It also describes how alterations in energy metabolism contribute to the development of heart dysfunction, and how optimization of Format: Hardcover.
Cardiac Energy Metabolism in Health and Disease describes the research advances that have been made in understanding what controls cardiac energy metabolism symposium molecular, transcriptional, and physiological levels.
It also describes how alterations in energy metabolism contribute to the development of heart dysfunction, and how optimization of Price: $ 3. Potential mechanisms for increased glucose reliance. A large number of studies in from increased energy metabolism to cardiac hypertrophy and failure book past two decades have demonstrated that the transcriptional regulation of genes involved in mitochondrial oxidative metabolism has changed significantly during the development of pathological hypertrophy and heart failure.
38 Down-regulation of peroxisome proliferator-activated receptor alpha (PPARα) and Cited by: It also describes how alterations in energy metabolism contribute to the development of heart dysfunction and how optimization of energy metabolism can be used to treat heart disease.
The topics covered include a discussion of the effects of myocardial ischemia, diabetes, obesity, hypertrophy, heart failure, and genetic disorders of.
It also describes how alterations in energy metabolism contribute to the development of heart dysfunction, and how optimization of energy metabolism can be used to treat heart disease.
The topics covered include a discussion of the effects of myocardial ischemia, diabetes, obesity, hypertrophy, heart failure, and genetic disorders of. While long-chain FFAs are the major source of energy in the normal adult mammalian heart, acquired disorders such as myocardial ischemia, heart failure and hypertrophy, but also inherited cardiac.
Cardiac hypertrophic adaptations are complex, and involve multiple cellular events and the mechanisms underlying the development of cardiac hypertrophy are not well understood.
Mitochondrial dysfunction has been indicated as a potential and important player in the development of cardiac by: Glucose metabolism and cardiac hypertrophy. Aside from increased reliance on glucose as an energy source, changes in other glucose metabolism pathways, e.g. 2. Glucose metabolism is increased in cardiac hypertrophy.
In the normal, adult heart, oxidation of fatty acids contributes the majority of carbon substrates to ATP generation. 6 However, the heart possesses tremendous metabolic flexibility highlighted by its ability to utilize glucose, lactate, ketones, and amino acids. Preference in substrate Cited by: Cardiac hypertrophy and the progressive development of cardiac failure are usually associated with suppression of fatty acid oxidation (FAO) and metabolic reversion to increase glucose utilization.
This shift in the source of energy from fatty acids to glucose is accompanied by a dramatic fall in the cardiac expression of genes involved in. Furthermore, energy transfer and energy status of the heart in hypertrophy and heart failure are discussed and the effect of treatments to improve energy status is presented.
In the end, we attempt together with Christian Schulze, Peter Kennel and Linda Peterson to illuminate the clinical relevance of metabolism and the current efforts and Author: Michael Schwarzer, Torsten Doenst.
Cardiac hypertrophy and failure are associated with increased activity of AMPK, which may be attributable to increased AMP/ATP ratio, ROS, or Ca 2+ load. Pharmacological interventions that further increase AMPK activity in HF models have resulted in reduced ventricular remodeling and improved cardiac function.
83, These findings suggest Cited by: Energy metabolism is a process that is central to cardiac health and disease. High ATP turnover in the myocardium is required to maintain contractile function, and ATP deficiency has been recognized as a hallmark of cardiac failure1.
ATP generation within the mitochondria involves oxidative decarboxylation of fatty acids and pyruvate and the Krebs cycle to generate reducing equivalents for Author: Thomas Pulinilkunnil, Petra Kienesberger, Jeevan Nagendran. Experimental Cardiac Hypertrophy and Heart Failure. Editors: Jacob, Ruthard (Ed.) Subcellular changes during cardiac hypertrophy and heart failure due to bacterial endocarditis.
Pages Increased uracil nucleotide metabolism during the induction of cardiac hypertrophy by β. The role of cardiac energy metabolism in cardiac hypertrophy and failure. cardiac muscle adapt to increased energy demand or compromised energy supply by reprogramming the network of genes whose products are necessary to match the production of energy to consumption.
Failure in this regulation leads to severe cardiac dysfunction and has Cited by: Glucose Metabolism in Cardiac Hypertrophy and Heart Failure Diem H. Tran PhD; Zhao V. Wang, PhD H eart failure is one of the leading causes of death worldwide and has been singled out as an emerging epidemic.1,2 With a 5-year survival rate of 50%, heart failure poses a tremendous burden on our economic and healthcare system.
Journal Article. Glucose metabolism and cardiac hypertrophy Stephen C. Kolwicz and Rong Tian. in Cardiovascular Research Published on behalf of European Society of Cardiology. Presented at the Experimental Biology Symposium Mitochondria and Energy Metabolism in Heart Failure, Hypertrophy and Remodeling, Orlando, Florida, USA, March/April The metabolic consequences of a sustained increase or decrease in the workload of the heart are surprisingly uniform and consist of a switch from the predominant oxidation Cited by: starvation in heart failure.
This review will focus on energy metabolism alterations in long-term chronic heart failure with only a few references to compensated hypertrophy when necessary. It will brieﬂy describe the energy metabolism of normal heart and skeletal muscles and their alterations in chronic heart by: Altered energy demand, shifts in substrate utilization and increased oxidative stress are observed in the hypertrophic heart.
Both a shift away from carbohydrate usage (i.e. insulin resistance) and a shift to carbohydrate usage (i.e. pressure loading) are associated with disturbed cardiomyocyte Ca(2+) homeostasis and the development of cardiac.
The beneficial effect of metabolic modulation of cardiac metabolism in HF has been attributed to the shift of energy production from free fatty acid oxidation to glucose oxidation, which leads to increased production of high-energy phosphates and therefore to greater cardiac and skeletal muscle efficiency.
22 The metabolic modulation through Cited by: Energy metabolism is a process that is central to cardiac health and disease. High turnover of ATP in the myocardium is required for efficient contractile function and ATP deficiency has been recognized as a hallmark of cardiac failure. ATP generation within the mitochondria involves oxidative decarboxylation of different nutrients including fatty acids, glucose, ketones, lactate and amino.Title: Sodium Ion Transporters as New Therapeutic Targets in Heart Failure VOLUME: 6 ISSUE: 4 Author(s):Antonius Baartscheer and Marcel M.G.J.
van Borren Affiliation:Center for Heart Failure Research, Department of Experimental Cardiology, Academic Medical Center Room K, University of Amsterdam, Meibergdreef 9 AZ Amsterdam, The Netherlands.