caa a22 4500 605479038 CHVBK 20210128100408.0 cr unu---uuuuu 210128e20150901xx s 000 0 eng 10.1007/s10741-015-9498-3 doi (NATIONALLICENCE)springer-10.1007/s10741-015-9498-3 The role of CaMKII in diabetic heart dysfunction [Elektronische Daten] [Lorna Daniels, James Bell, Lea Delbridge, Fiona McDonald, Regis Lamberts, Jeffrey Erickson] Diabetes mellitus (DM) is an increasing epidemic that places a significant burden on health services worldwide. The incidence of heart failure (HF) is significantly higher in diabetic patients compared to non-diabetic patients. One underlying mechanism proposed for the link between DM and HF is activation of calmodulin-dependent protein kinase (CaMKIIδ). CaMKIIδ mediates ion channel function and Ca2+ handling during excitation-contraction and excitation-transcription coupling in the myocardium. CaMKIIδ activity is up-regulated in the myocardium of diabetic patients and mouse models of diabetes, where it promotes pathological signaling that includes hypertrophy, fibrosis and apoptosis. Pharmacological inhibition and knockout models of CaMKIIδ have shown some promise of a potential therapeutic benefit of CaMKIIδ inhibition, with protection against cardiac hypertrophy and apoptosis reported. This review will highlight the pathological role of CaMKIIδ in diabetes and discuss CaMKIIδ as a therapeutic target in DM, and also the effects of exercise on CaMKIIδ. Springer Science+Business Media New York, 2015 CaMKII nationallicence Diabetes mellitus nationallicence Diabetic heart dysfunction nationallicence Heart failure nationallicence Exercise nationallicence Daniels Lorna Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand aut Bell James Department of Physiology, University of Melbourne, Melbourne, VIC, Australia aut Delbridge Lea Department of Physiology, University of Melbourne, Melbourne, VIC, Australia aut McDonald Fiona Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand aut Lamberts Regis Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand aut Erickson Jeffrey Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand aut Heart Failure Reviews Springer US; http://www.springer-ny.com 20/5(2015-09-01), 589-600 1382-4147 20:5<589 2015 20 10741 https://doi.org/10.1007/s10741-015-9498-3 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s10741-015-9498-3 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Daniels Lorna Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand aut NATIONALLICENCE 700 1- Bell James Department of Physiology, University of Melbourne, Melbourne, VIC, Australia aut NATIONALLICENCE 700 1- Delbridge Lea Department of Physiology, University of Melbourne, Melbourne, VIC, Australia aut NATIONALLICENCE 700 1- McDonald Fiona Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand aut NATIONALLICENCE 700 1- Lamberts Regis Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand aut NATIONALLICENCE 700 1- Erickson Jeffrey Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand aut NATIONALLICENCE 773 0- Heart Failure Reviews Springer US; http://www.springer-ny.com 20/5(2015-09-01), 589-600 1382-4147 20:5<589 2015 20 10741