scholarly journals T-tubule remodeling and increased heterogeneity of calcium release during the progression to heart failure in intact rat ventricle

2017 ◽  
Vol 5 (24) ◽  
pp. e13540 ◽  
Author(s):  
Jasleen K. Singh ◽  
Varderes Barsegyan ◽  
Nikhil Bassi ◽  
William Marszalec ◽  
Shannon Tai ◽  
...  
2012 ◽  
Vol 140 (6) ◽  
pp. 250-254
Author(s):  
Masafumi Yano ◽  
Takeshi Yamamoto ◽  
Shigeki Kobayashi ◽  
Masunori Matsuzaki

2012 ◽  
Vol 102 (3) ◽  
pp. 551a
Author(s):  
Jennifer A. Rochira ◽  
Karim Roder ◽  
Weiyan Li ◽  
Radmila Terentyeva ◽  
Yukiko Kunitomo ◽  
...  

Circulation ◽  
2003 ◽  
Vol 107 (3) ◽  
pp. 477-484 ◽  
Author(s):  
Masafumi Yano ◽  
Shigeki Kobayashi ◽  
Masateru Kohno ◽  
Masahiro Doi ◽  
Takahiro Tokuhisa ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Jean-Pierre Benitah ◽  
Romain Perrier ◽  
Jean-Jacques Mercadier ◽  
Laetitia Pereira ◽  
Ana M. Gómez

Heart Failure (HF) is defined as the inability of the heart to efficiently pump out enough blood to maintain the body's needs, first at exercise and then also at rest. Alterations in Ca2+ handling contributes to the diminished contraction and relaxation of the failing heart. While most Ca2+ handling protein expression and/or function has been shown to be altered in many models of experimental HF, in this review, we focus in the sarcoplasmic reticulum (SR) Ca2+ release channel, the type 2 ryanodine receptor (RyR2). Various modifications of this channel inducing alterations in its function have been reported. The first was the fact that RyR2 is less responsive to activation by Ca2+ entry through the L-Type calcium channel, which is the functional result of an ultrastructural remodeling of the ventricular cardiomyocyte, with fewer and disorganized transverse (T) tubules. HF is associated with an elevated sympathetic tone and in an oxidant environment. In this line, enhanced RyR2 phosphorylation and oxidation have been shown in human and experimental HF. After several controversies, it is now generally accepted that phosphorylation of RyR2 at the Calmodulin Kinase II site (S2814) is involved in both the depressed contractile function and the enhanced arrhythmic susceptibility of the failing heart. Diminished expression of the FK506 binding protein, FKBP12.6, may also contribute. While these alterations have been mostly studied in the left ventricle of HF with reduced ejection fraction, recent studies are looking at HF with preserved ejection fraction. Moreover, alterations in the RyR2 in HF may also contribute to supraventricular defects associated with HF such as sinus node dysfunction and atrial fibrillation.


PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109309 ◽  
Author(s):  
Marino DiFranco ◽  
Marbella Quiñonez ◽  
Perry Shieh ◽  
Gregg C. Fonarow ◽  
Daniel Cruz ◽  
...  

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