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From eggs to hearts: what is the link between cyclic ADP-ribose and ryanodine receptors?

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Elisa Venturi, Samantha Jane Pitt, Elena Galfre, Rebecca Sitsapesan

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It was first proposed that cyclic ADP-ribose (cADPR) could activate ryanodine receptors (RyR) in 1991. Following a subsequent report that cADPR could activate cardiac RyR (RyR2) reconstituted into artificial membranes and stimulate Ca2+-release from isolated cardiac SR, there has been a steadily mounting stockpile of publications proclaiming the physiological and pathophysiological importance of cADPR in the cardiovascular system. It was only 2 years earlier, in 1989, that cADPR was first identified as the active metabolite of nicotinamide adenine dinucleotide (NAD), responsible for triggering the release of Ca2+ from crude homogenates of sea urchin eggs. Twenty years later, can we boast of being any closer to unraveling the mechanisms by which cADPR modulates intracellular Ca2+ -release? This review sets out to examine the mechanisms underlying the effects of cADPR and ask whether cADPR is an important signaling molecule in the heart.



Original languageEnglish
Pages (from-to)109-16
JournalCardiovascular Therapeutics
Issue number2
Publication statusPublished - 2012

    Research areas

  • Arrhythmia, Heart Disease, Molecular Cardiobiology

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