https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13385 Wed 11 Apr 2018 17:04:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14428 Wed 11 Apr 2018 13:17:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27466 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 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.]]> Sat 24 Mar 2018 07:32:43 AEDT ]]>