Journal
CARDIOVASCULAR THERAPEUTICS
Volume 30, Issue 2, Pages 109-116Publisher
WILEY
DOI: 10.1111/j.1755-5922.2010.00236.x
Keywords
Arrhythmias; Ischemic heart disease; Molecular cardiobiology; Vascular biology
Funding
- British Heart Foundation [FS/08/069/25929] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available