The role of CaMKII in diabetic heart dysfunction

Verfasser / Beitragende:
[Lorna Daniels, James Bell, Lea Delbridge, Fiona McDonald, Regis Lamberts, Jeffrey Erickson]
Ort, Verlag, Jahr:
2015
Enthalten in:
Heart Failure Reviews, 20/5(2015-09-01), 589-600
Format:
Artikel (online)
ID: 605479038
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024 7 0 |a 10.1007/s10741-015-9498-3  |2 doi 
035 |a (NATIONALLICENCE)springer-10.1007/s10741-015-9498-3 
245 0 4 |a The role of CaMKII in diabetic heart dysfunction  |h [Elektronische Daten]  |c [Lorna Daniels, James Bell, Lea Delbridge, Fiona McDonald, Regis Lamberts, Jeffrey Erickson] 
520 3 |a 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. 
540 |a Springer Science+Business Media New York, 2015 
690 7 |a CaMKII  |2 nationallicence 
690 7 |a Diabetes mellitus  |2 nationallicence 
690 7 |a Diabetic heart dysfunction  |2 nationallicence 
690 7 |a Heart failure  |2 nationallicence 
690 7 |a Exercise  |2 nationallicence 
700 1 |a Daniels  |D Lorna  |u Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand  |4 aut 
700 1 |a Bell  |D James  |u Department of Physiology, University of Melbourne, Melbourne, VIC, Australia  |4 aut 
700 1 |a Delbridge  |D Lea  |u Department of Physiology, University of Melbourne, Melbourne, VIC, Australia  |4 aut 
700 1 |a McDonald  |D Fiona  |u Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand  |4 aut 
700 1 |a Lamberts  |D Regis  |u Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand  |4 aut 
700 1 |a Erickson  |D Jeffrey  |u Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand  |4 aut 
773 0 |t Heart Failure Reviews  |d Springer US; http://www.springer-ny.com  |g 20/5(2015-09-01), 589-600  |x 1382-4147  |q 20:5<589  |1 2015  |2 20  |o 10741 
856 4 0 |u https://doi.org/10.1007/s10741-015-9498-3  |q text/html  |z Onlinezugriff via DOI 
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950 |B NATIONALLICENCE  |P 856  |E 40  |u https://doi.org/10.1007/s10741-015-9498-3  |q text/html  |z Onlinezugriff via DOI 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Daniels  |D Lorna  |u Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Bell  |D James  |u Department of Physiology, University of Melbourne, Melbourne, VIC, Australia  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Delbridge  |D Lea  |u Department of Physiology, University of Melbourne, Melbourne, VIC, Australia  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a McDonald  |D Fiona  |u Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Lamberts  |D Regis  |u Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Erickson  |D Jeffrey  |u Department of Physiology, University of Otago, PO Box 56, Dunedin, New Zealand  |4 aut 
950 |B NATIONALLICENCE  |P 773  |E 0-  |t Heart Failure Reviews  |d Springer US; http://www.springer-ny.com  |g 20/5(2015-09-01), 589-600  |x 1382-4147  |q 20:5<589  |1 2015  |2 20  |o 10741