Mechanisms of SR calcium release in healthy and failing human hearts

Biophysics Reviews
K Walweel, D R Laver

Abstract

Normal heart contraction and rhythm relies on the proper flow of calcium ions (Ca2+) 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 Ca2+ channels to open and allow Ca2+ to enter the cytoplasm. The subsequent increase in cytoplasmic Ca2+ concentration activates calcium release channels (RyR2) located at specialised Ca2+ release sites in the sarcoplasmic reticulum (SR), which serves as an intracellular Ca2+ store. Animal models have provided valuable insights into how intracellular Ca2+ transport mechanisms are altered in human heart failure. The aim of this review is to examine how Ca2+ release sites are remodelled in heart failure and how this affects intracellular Ca2+ transport with an emphasis on Ca2+ release mechanisms in the SR. Current knowledge on how heart failure alters the regulation of RyR2 by Ca2+ and Mg2+ and how these mechanisms control the activity of RyR2 in the confines of the Ca2+ release sites is reviewed.

References

Jan 1, 1988·Proceedings of the National Academy of Sciences of the United States of America·L HymelH Schindler
Jul 22, 1982·The New England Journal of Medicine·M R BristowE B Stinson
Sep 27, 1984·The New England Journal of Medicine·J N CohnT Rector
Nov 1, 1993·The Journal of Physiology·D F Van Helden
Feb 1, 1994·The Journal of Membrane Biology·R Sitsapesan, A J Williams
Sep 1, 1995·The Journal of Membrane Biology·D R LaverA F Dulhunty
Apr 1, 1997·The Journal of Membrane Biology·D R LaverA F Dulhunty
Jul 1, 1997·Physiological Reviews·C Franzini-Armstrong, F Protasi
Oct 6, 1997·The Journal of Membrane Biology·R Sitsapesan, A J Williams
Mar 21, 1998·Journal of the American College of Cardiology·M C HaigneyH Silverman
Apr 13, 1999·Journal of Molecular and Cellular Cardiology·R H SchwingerE Erdmann
Mar 29, 2001·Journal of Molecular and Cellular Cardiology·A R Marks
Jul 5, 2001·Journal of Molecular and Cellular Cardiology·R DashE G Kranias
Sep 20, 2001·Proceedings of the National Academy of Sciences of the United States of America·J SunG Meissner
Jan 24, 2002·Nature·Donald M Bers
Sep 18, 2002·Journal of Molecular and Cellular Cardiology·Gerd Hasenfuss, Burkert Pieske
Sep 28, 2002·Molecular and Cellular Biochemistry·Sajal ChakrabortiSamarendranath Ghosh
Nov 29, 2002·Circulation Research·D A Eisner, A W Trafford
Nov 29, 2002·Circulation Research·Ming Tao JiangHéctor H Valdivia
Feb 11, 2003·The Journal of Physiology·Dirk F van Helden, Mohammad S Imtiaz
Feb 26, 2003·Circulation Research·Valentino PiacentinoSteven R Houser

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Citations

Dec 31, 2019·SLAS Discovery·Juliana Maynard, Philippa Hart
Jun 15, 2019·Biomolecules·Jelena MilicJürgen Bernhagen
Sep 8, 2020·Toxicological Sciences : an Official Journal of the Society of Toxicology·Kim M TruongIsaac N Pessah
Dec 5, 2020·Heart Failure Reviews·Amir FathiJagdeep S Singh

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