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Matsuzaki Masanori

Affiliate Master Yamaguchi University

Ryanodine Receptor Defects in Heart Failure

The bulletin of the Yamaguchi Medical School Volume 53 Issue 3-4 Page 19-23
published_at 2006-12
A050053000301.pdf
[fulltext] 626 KB
Title
Ryanodine Receptor Defects in Heart Failure
Creators Oda Tetsuro
Creators Yano Masafumi
Creators Matsuzaki Masunori
Source Identifiers
Creator Keywords
heart failure ryanodine receptor excitation-contraction coupling domain interaction
Abnormal regulation of intracellular Ca2- by sarcoplasmic reticulum plays a part in the mechanism underlying contractile and relaxation dysfunction in heart failure (HF). The protein-kinase-A-mediated hyperphosphorylation of ryanodine receptors in the sarcoplasmic reticulum has been shown to cause the dissociation of FKBP12.6 (also known as calstabin-2) from ryanodien receptors in HF. In addition, several disease-linked mutations in the ryanodine receptors have been reported in patients with catecholaminergic polymorphic ventricular tachycardia or arrhythmogenic right ventricular cardiomyopathy type2. The unique distribution of these mutation sites has led to the concept that the interaction among the putative regulatory domains within the ryanodine receptors has a key role in regulating channel opening. The knowledge gained from various studies of ryanodine receptors under pathologic conditions might lead to the development of new pharmacological or genetic strategies for the treatment of HF or cardiac arrhythmia. In this review, we focus on the role of the Ca2--release channel, the ryanodine receptor, in the pathogenesis of HF and fatal arrhythmia, and the possibility of developing new therapeutic strategies by targeting this receptor.
Subjects
医学 ( Other)
Languages eng
Resource Type departmental bulletin paper
Publishers Yamaguchi University School of Medicine
Date Issued 2006-12
File Version Version of Record
Access Rights open access
Relations
[isVersionOf] [URI]http://ds.cc.yamaguchi-u.ac.jp/~bulletin/index.html
Schools 医学部