Mechanisms of SR calcium release in healthy and failing human hearts

Normal heart contraction and rhythm relies on the proper flow of calcium ions (Ca 2+ ) into cardiac cells and between their intracellular organelles, and any disruption can lead to arrhythmia and sudden cardiac death. Electrical excitation of the surface membrane activates voltage-dependent L-type C...

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Bibliographic Details
Published in:Biophysical reviews 2015-03, Vol.7 (1), p.33-41
Main Authors: Walweel, K., Laver, D. R.
Format: Article
Language:English
Subjects:
Biochemistry
Biological and Medical Physics
Biological Techniques
Biomedical and Life Sciences
Biophysics
Cell Biology
Life Sciences
Membrane Biology
Nanotechnology
Review
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Summary:Normal heart contraction and rhythm relies on the proper flow of calcium ions (Ca 2+ ) into cardiac cells and between their intracellular organelles, and any disruption can lead to arrhythmia and sudden cardiac death. Electrical excitation of the surface membrane activates voltage-dependent L-type Ca 2+ channels to open and allow Ca 2+ to enter the cytoplasm. The subsequent increase in cytoplasmic Ca 2+ concentration activates calcium release channels (RyR2) located at specialised Ca 2+ release sites in the sarcoplasmic reticulum (SR), which serves as an intracellular Ca 2+ store. Animal models have provided valuable insights into how intracellular Ca 2+ transport mechanisms are altered in human heart failure. The aim of this review is to examine how Ca 2+ release sites are remodelled in heart failure and how this affects intracellular Ca 2+ transport with an emphasis on Ca 2+ release mechanisms in the SR. Current knowledge on how heart failure alters the regulation of RyR2 by Ca 2+ and Mg 2+ and how these mechanisms control the activity of RyR2 in the confines of the Ca 2+ release sites is reviewed.
ISSN:1867-2450
1867-2469
DOI:10.1007/s12551-014-0152-4