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Ryanodine receptor as a new therapeutic target of heart failure and lethal arrhythmia Yano MCirc J 2008[Apr]; 72 (4): 509-14Abnormal intracellular Ca(2+) handling by the sarcoplasmic reticulum (SR) is a critical factor in the development of heart failure (HF). Not only decreased Ca(2+) uptake, but also uncoordinated Ca(2+) release plays a significant role in contractile and relaxation dysfunction. Spontaneous Ca(2+) release through ryanodine receptor (RyR) 2, a huge tetrameric protein, during diastole leads to a decrease in the SR Ca(2+) content, and also triggers delayed after depolarization that is a substrate for lethal arrhythmia. Several disease-linked mutations of RyR have been reported in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) or arrhythmogenic right ventricular cardiomyopathy type 2 (ARVC2). The unique distribution of these mutation sites has lead to the concept that an interaction among the putative regulatory domains within RyR may play a key role in regulating channel opening, and that there seems to be a common abnormality in the channel disorder of HF and CPVT/ARVC2. Recent knowledge gained from pathological conditions may lead to the development of a new therapeutic strategy for the treatment of HF or cardiac arrhythmia.|Animals[MESH]|Arrhythmias, Cardiac/genetics/*physiopathology/*therapy[MESH]|Calcium Signaling[MESH]|Calcium-Calmodulin-Dependent Protein Kinase Type 2/physiology[MESH]|Heart Failure/genetics/*physiopathology/*therapy[MESH]|Humans[MESH]|Ion Channel Gating[MESH]|Models, Cardiovascular[MESH]|Models, Molecular[MESH]|Mutation[MESH]|Protein Interaction Domains and Motifs[MESH]|Ryanodine Receptor Calcium Release Channel/chemistry/genetics/*physiology[MESH] |
