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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Biochim Biophys Acta. 2013 Jun 14;1832(12):10.1016/j.bbadis.2013.06.008. doi: 10.1016/j.bbadis.2013.06.008

Figure 1.

Figure 1

Schematic representation of changes in Type 2 Ryanodine receptors (RyR2) and related proteins in heart failure (HF). Left, represents Ca2+ handling in a cell from normal heart, and right, represents Ca2+ handling in a cell from a failing heart. 1) shows increased RyR2 activity represented by a wide open RyR2 due to post-translational modification by increased protein kinase A (PKA) and Ca2+/CaM-dependent protein kinase II (CaMKII) activity, reduced protein phosphatases (PP) 1 and PP 2A activity, reduced junctophilin 2 (JPH2) leading to abnormalities in T-tubule structure and increased oxidation by reactive oxygen species (ROS), 2) represents complex changes in L-type Ca2+ channel (LTCC) as discussed in the text, 3) represents reduced SR/ER Ca2+-ATPase (SERCA2a) activity and corresponding increased phospholamban (PLN) and Sarcolipin (SLN) activity, and 4) represents increased Na+/Ca2+ exchanger (NCX) activity, in heart failure. ↑ represents increase and ↓ represents decrease.