Search results: Found 8

Listing 1 - 8 of 8
Sort by
Cardiac Remodeling: New Insights in Physiological and Pathological Adaptations

Authors: ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889453313 Year: Pages: 117 DOI: 10.3389/978-2-88945-331-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2018-02-27 16:16:45
License:

Loading...
Export citation

Choose an application

Abstract

The effective management of Cardiac remodeling(CR), remains a major challenge. Heart failure remains the leading cause of death in industrialized countries. Yet, despite the enormity of the problem, effective therapeutic interventions remain elusive. In fact, several initially promising agents were found to decrease mortality in patients recovering from myocardial infarction. Cardiac remodeling is defined as molecular and interstitial changes, manifested clinically by changes in size, mass , geometry and function of the heart in response to certain aggression. Initially, ventricular remodeling aims to maintain stable cardiac function in situations of aggression.

CaMKII in Cardiac Health and Disease

Authors: --- --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192991 Year: Pages: 165 DOI: 10.3389/978-2-88919-299-1 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Medicine (General) --- Therapeutics --- Science (General)
Added to DOAB on : 2015-12-10 11:59:07
License:

Loading...
Export citation

Choose an application

Abstract

The calcium-calmodulin dependent protein kinases (CaMKs) are a broadly expressed family of calcium-sensitive intracellular kinases, which are responsible for transducing cytosolic calcium signals into phosphorylation-based regulation of proteins and physiological functions. As the multifunctional member of the family, CaMKII has become the most prominent for its roles in the central nervous system and heart, where it controls a diverse range of calcium-dependent processes; from learning and memory at the neuronal synapse, to cellular growth and death in the myocardium. In the heart, CaMKII directly regulates many of the most important ion channels and calcium handling proteins, and controls the expression of an ever-increasing number of transcripts and their downstream products. Functionally, these actions are thought to orchestrate many of the electrophysiologic and contractile adaptations to common cardiac stressors, such as rapid pacing, chronic adrenergic stimulation, and oxidative challenge. In the context of disease, CaMKII has been shown to contribute to a remarkably wide variety of cardiac pathologies, of which heart failure (HF) is the most conspicuous. Hyperactivity of CaMKII is an established contributor to pathological cardiac remodeling, and is widely thought to directly promote arrhythmia and contractile dysfunction during HF. Moreover, several non-failing arrhythmia-susceptible phenotypes, which result from specific genetic channelopathies, functionally mimic constitutive channel phosphorylation by CaMKII. Because CaMKII contributes to both the acute and chronic manifestations of major cardiac diseases, but may be only minimally required for homeostasis in the absence of chronic stress, it has come to be one of the most promising therapeutic drug targets in cardiac biology. Thus, development of more specific and deliverable small molecule antagonists remains a key priority for the field. Here we provide a selection of articles to summarize the state of our knowledge regarding CaMKII in cardiac health and disease, with a particular view to highlighting recent developments in CaMKII activation, and new targets in CaMKII-mediated control of myocyte physiology.

Computer assisted optimization of cardiac resynchronization therapy

Author:
Book Series: Karlsruhe transactions on biomedical engineering / Ed.: Universität Karlsruhe (TH) / Institute of Biomedical Engineering ISSN: 18645933 ISBN: 9783866443600 Year: Volume: 6 Pages: IV, 293 p. DOI: 10.5445/KSP/1000011293 Language: ENGLISH
Publisher: KIT Scientific Publishing
Subject: Technology (General)
Added to DOAB on : 2019-07-30 20:02:02
License:

Loading...
Export citation

Choose an application

Abstract

The efficacy of cardiac resynchronization therapy (CRT) through biventricular pacing (BVP) has been demonstrated by numerous studies in patients suffering from congestive heart failure. In order to achieve a guideline for optimal treatment with BVP devices, an automated non-invasive strategy based on an electrophysiological computer model of the heart is presented. The presented research investigates an off-line optimization algorithm based on different electrode positioning and timing delays.

The adrenergic system in cardiovascular physiology and pathophysiology

Author:
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193981 Year: Pages: 85 DOI: 10.3389/978-2-88919-398-1 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2015-12-10 11:59:06
License:

Loading...
Export citation

Choose an application

Abstract

Cardiovascular diseases pose an enormous clinical challenge, remaining the most common cause of death in the world. ß-adrenoceptors play an important role on cardiac, vascular and/or endothelial function at a cellular level with relevant applications in several cardiovascular diseases, such as heart failure and hypertension. G protein– coupled receptors (GPCRs), including ß-adrenergic receptors, constitute the most ubiquitous superfamily of plasma membrane receptors and represent the single most important type of therapeutic drug target. Sympathetic nervous system hyperactivity, which characterizes several cardiovascular diseases, such as heart failure and hypertension, as well as physiological ageing, has been proved to exert in the long-term detrimental effects in a wide range of cardiovascular diseases. Acutely, sympathetic hyperactivity represents the response to an insult to the myocardium, aiming to compensate for decreased cardiac output. This process involves the activation of beta-adrenergic receptors by catecholamine with consequent heart rate and cardiac contractility increase. However, long-term exposure of the heart to elevated norepinephrine and epinephrine levels, originating from sympathetic nerve endings and chromaffin cells of the adrenal gland, results in further progressive deterioration in cardiac structure and function. At the molecular level, sustained sympathetic nervous system hyperactivity is responsible for several alterations including altered beta-adrenergic receptor signaling and function (down-regulation/ desensitization). Moreover, the detrimental effects of catecholamine affect also the function of different cell types including, but not limited to, endothelial cells, fibroblasts and smooth muscle cells. Thus, the success of beta-blocker therapy is due, at least in part, to the protection of the heart and the vasculature from the noxious effects of augmented catecholamine levels. The research topic aimed to support the progress towards understanding the role of sympathetic nervous system under physiological conditions, and the contribution of its hyperactivity in the pathogenesis and progression of cardiovascular diseases.

Carotid Body: A New Target for Rescuing Neural Control of Cardiorespiratory Balance in Disease

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199433 Year: Pages: 134 DOI: 10.3389/978-2-88919-943-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2016-01-19 14:05:46
License:

Loading...
Export citation

Choose an application

Abstract

The carotid body (CB) is in charge of adjusting ventilatory and cardiovascular function during changes in arterial blood gases. Regardless this essential function, the CB has been implicated in the sensing of other physiological signals such as changes in blood flow and glucose levels. More important, malfunction of the CB chemoreceptors has been associated with the progression and deterioration of several disease states such as hypertension, heart failure, renal failure, insulin resistance, diabetes and sleep apnea. Although the mechanisms involved in the alterations of the CB function in pathophysiology are currently under intense research, the development of therapeutic approaches to restore normal CB chemoreflex function remains unsolved. Recent studies showing the effect of CB denervation in pathophysiology have unveiled a key role of these arterial chemoreceptors in the development of autonomic imbalance and respiratory disturbances, and suggest that targeting the CB could represent a novel strategy to improve disease outcome. Unfortunately, classical pharmacotherapy intended to normalize CB function may be hard to establish since several cellular pathways are involved in the CB dysfunction. Augmented levels of angiotensin II, endothelin-1, cytokines and free radicals along with decreases in nitric oxide had all been related to the CB dysfunction. Moreover, changes in expression of angiotensin receptors, nitric oxide synthases and cytokines that take place within the CB tissue in pathological states also contribute to the enhanced CB chemoreflex drive. It has been shown in heart failure, hypertension and obstructive sleep apnea that the CB becomes tonically hyper-reactive. During the progression of the disease this CB chemosensory facilitation process induces central nervous system plasticity. The altered autonomic-respiratory control leads to increased cardiorespiratory distress and the deterioration of the condition. The focus of this e-book will be to cover the role of the CB in pathophysiology and to provide new evidence of the pathways involved in the maladaptive potentiation of the CB chemoreflex function. In memory of Professor Mashiko Shirahata and Professor Constancio Gonzalez.

The Adrenergic System in Cardiovascular Physiology and Pathophysiology, 2nd Edition

Author:
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197316 Year: Pages: 78 DOI: 10.3389/978-2-88919-731-6 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
License:

Loading...
Export citation

Choose an application

Abstract

Cardiovascular diseases pose an enormous clinical challenge, remaining the most common cause of death in the world. ß-adrenoceptors play an important role on cardiac, vascular and/or endothelial function at a cellular level with relevant applications in several cardiovascular diseases, such as heart failure and hypertension. G protein– coupled receptors (GPCRs), including ß-adrenergic receptors, constitute the most ubiquitous superfamily of plasma membrane receptors and represent the single most important type of therapeutic drug target. Sympathetic nervous system hyperactivity, which characterizes several cardiovascular diseases, such as heart failure and hypertension, as well as physiological ageing, has been proved to exert in the long-term detrimental effects in a wide range of cardiovascular diseases. Acutely, sympathetic hyperactivity represents the response to an insult to the myocardium, aiming to compensate for decreased cardiac output. This process involves the activation of beta-adrenergic receptors by catecholamine with consequent heart rate and cardiac contractility increase. However, long-term exposure of the heart to elevated norepinephrine and epinephrine levels, originating from sympathetic nerve endings and chromaffin cells of the adrenal gland, results in further progressive deterioration in cardiac structure and function. At the molecular level, sustained sympathetic nervous system hyperactivity is responsible for several alterations including altered beta-adrenergic receptor signaling and function (down-regulation/ desensitization). Moreover, the detrimental effects of catecholamine affect also the function of different cell types including, but not limited to, endothelial cells, fibroblasts and smooth muscle cells. Thus, the success of beta-blocker therapy is due, at least in part, to the protection of the heart and the vasculature from the noxious effects of augmented catecholamine levels. The research topic aimed to support the progress towards understanding the role of sympathetic nervous system under physiological conditions, and the contribution of its hyperactivity in the pathogenesis and progression of cardiovascular diseases.

Function of Renal Sympathetic Nerves

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452958 Year: Pages: 96 DOI: 10.3389/978-2-88945-295-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2018-02-27 16:16:44
License:

Loading...
Export citation

Choose an application

Abstract

Sympathetic overactivity is associated with the development of hypertension. Renal denervation (RDN) prevents or delays hypertension in a variety of animal models, which laid the groundwork for the introduction of RDN as a clinical therapy in humans. In 2007, a novel, minimally invasive RDN ablation catheter was first trialled in hypertensive patients, with a 93% success rate of lowering blood pressure for at least three years post-RDN. However, a large scale, sham-controlled clinical trial (Symplicity HTN -3) failed to show reductions in BP greater than sham. The aim of this research topic was to evaluate the efficacy and safety of RDN, to explore the contribution of both afferent and efferent renal nerve activity to hypertension and non-hypertension disorders, and to stimulate future research to better understand the function of the renal nerves and the effects of RDN by highlighting gaps in knowledge.

Second hand smoke and COPD: lessons from animal studies

Authors: --- ---
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193165 Year: Pages: 91 DOI: 10.3389/978-2-88919-316-5 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
License:

Loading...
Export citation

Choose an application

Abstract

Cigarette smoke exposure is the key initiator of chronic inflammation, alveolar destruction, and the loss of alveolar blood vessels that lead to the development of chronic obstructive pulmonary disease (COPD) which is comprised of emphysema and chronic bronchitis. Exposure to secondhand smoke (SHS) is the major risk factor for non-smokers to develop emphysema. While the first-hand smoke is directly inhaled by smokers, passive smoking occurs when non-smokers are involuntary exposed to environmental tobacco smoke also known as second hand smoke (SHS). SHS is a mixture of 2 forms of smoke that come from burning tobacco: side stream smoke (smoke that comes from the end of a lit cigarette, pipe, or cigar) and mainstream smoke (smoke that is exhaled by a smoker). These two types of smoke have basically the same composition, however in SHS many toxic components are more concentrated than in first-hand smoke, therefore more hazardous for people’s health. Several pathological events have been implicated in the development of SHS-induced COPD, but many aspects of this pathology remain poorly understood halting the development of new advanced treatments for this detrimental disease. In this respect we have welcomed leading investigators in the field to share their research findings and provide their thoughts regarding the mechanisms of the SHS exposure-induced immune responses and inflammatory mechanisms of lung destruction in SHS-induced COPD and related comorbidities.

Listing 1 - 8 of 8
Sort by
Narrow your search

Publisher

Frontiers Media SA (7)

KIT Scientific Publishing (1)


License

CC by (7)

CC by-nc-nd (1)


Language

english (8)


Year
From To Submit

2017 (2)

2016 (1)

2015 (3)

2014 (1)

2009 (1)