LEADER 04128nam 2200589 450 001 9910137203503321 005 20230621140731.0 010 $a9782889192991$b(ebook) 035 $a(CKB)3710000000526094 035 $a(SSID)ssj0001666232 035 $a(PQKBManifestationID)16454582 035 $a(PQKBTitleCode)TC0001666232 035 $a(PQKBWorkID)15000658 035 $a(PQKB)11627453 035 $a(WaSeSS)IndRDA00056249 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/42609 035 $a(EXLCZ)993710000000526094 100 $a20160829d2014 uy 0 101 0 $aeng 135 $aur||#|||||||| 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aCaMKII in cardiac health and disease /$ftopic editors: Eleonora Grandi, Andrew G. Edwards, Anthony W. Herren and Donald M. Bers 210 $cFrontiers Media SA$d2014 210 31$aFrance :$cFrontiers Media SA,$d2014 215 $a1 online resource (165 pages) $cdigital, PDF file(s) 225 0 $aFrontiers Research Topics,$x1664-8714 300 $aBibliographic Level Mode of Issuance: Monograph 320 $aIncludes bibliographical references. 330 $aThe 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. 606 $aCardiovascular Diseases$2HILCC 606 $aMedicine$2HILCC 606 $aHealth & Biological Sciences$2HILCC 610 $aPhosphorylation 610 $aIon Channels 610 $aCalcium 610 $aarrhythmia 610 $aHeart Failure 610 $aHypertrophy 615 7$aCardiovascular Diseases 615 7$aMedicine 615 7$aHealth & Biological Sciences 700 $aAndrew G Edwards$4auth$01367189 702 $aHerren$b Anthony W 702 $aBers$b D. M 702 $aEdwards$b Andrew G 801 0$bPQKB 801 2$bUkMaJRU 912 $a9910137203503321 996 $aCaMKII in cardiac health and disease$93389919 997 $aUNINA