Novel aspects of excitation–contraction coupling in heart failure
Author:
Publisher
Springer Science and Business Media LLC
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Link
http://link.springer.com/content/pdf/10.1007/s00395-013-0360-2.pdf
Reference133 articles.
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3. Antos CL, Frey N, Marx SO, Reiken S, Gaburjakova M, Richardson JA, Marks AR, Olson EN (2001) Dilated cardiomyopathy and sudden death resulting from constitutive activation of protein kinase A. Circ Res 89:997–1004. doi: 10.1161/hh2301.100003
4. Ashpole NM, Herren AW, Ginsburg KS, Brogan JD, Johnson DE, Cummins TR, Bers DM, Hudmon A (2012) Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates cardiac sodium channel NaV1.5 gating by multiple phosphorylation sites. J Biol Chem 287:19856–19869. doi: 10.1074/jbc.M111.322537
5. Baartscheer A, Schumacher CA, van Borren MM, Belterman CN, Coronel R, Fiolet JW (2003) Increased Na+/H+-exchange activity is the cause of increased [Na+]i and underlies disturbed calcium handling in the rabbit pressure and volume overload heart failure model. Cardiovasc Res 57:1015–1024. doi: 10.1016/S0008-6363(02)00809-X
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