Elisa Venturi, Samantha Pitt, Elena Galfré, Rebecca Sitsapesan
School of Physiology and Pharmacology, British Heart Institute and NSQI, University of Bristol, University Walk, Bristol, UK.
Cardiovascular therapeutics 2012 AprIt 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. © 2010 Blackwell Publishing Ltd.
Elisa Venturi, Samantha Pitt, Elena Galfré, Rebecca Sitsapesan. From eggs to hearts: what is the link between cyclic ADP-ribose and ryanodine receptors? Cardiovascular therapeutics. 2012 Apr;30(2):109-16
PMID: 21176119
View Full Text