Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

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.

Fibrosis --- Heart Failure --- Physiology --- Inflammation --- Cardiac Remodeling

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

immunity --- inflammation --- cardiovascular disease --- arrhythmias --- heart failure --- myocarditis --- valve disease

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

nanotechnology --- cardiovascular --- regenerative medicine --- nanoparticle --- tissue engineering --- heart failure

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

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 remodelling, and is widely thought to directly promote arrhythmia and contractile dysfunction during HF. CaMKII is also ubiquitous in non-failing arrhythmia-susceptible phenotypes, several of which result from specific channelopathies that mimic constitutive channel phosphorylation. 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.

Cardiovascular Diseases --- Medicine --- Health & Biological Sciences --- Phosphorylation --- Ion Channels --- Calcium --- arrhythmia --- Heart Failure --- Hypertrophy

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

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.

atherosclerosis --- heart failure --- renal denervation --- renal sympathetic nerves --- kidney disease --- hypertension