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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 Ca(2+) -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 Ca(2+) 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 Ca(2+) -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 publication

DOI

10.1111/j.1755-5922.2010.00236.x

Type

Journal article

Journal

Cardiovasc Ther

Publication Date

04/2012

Volume

30

Pages

109 - 116

Keywords

Animals, Calcium Signaling, Cyclic ADP-Ribose, Fertilization, Heart, Humans, NADP, Ovum, Protein Binding, Ryanodine Receptor Calcium Release Channel, Sea Urchins, Tacrolimus Binding Proteins