期刊
CARDIOVASCULAR THERAPEUTICS
卷 30, 期 2, 页码 109-116出版社
WILEY
DOI: 10.1111/j.1755-5922.2010.00236.x
关键词
Arrhythmias; Ischemic heart disease; Molecular cardiobiology; Vascular biology
资金
- British Heart Foundation [FS/08/069/25929] Funding Source: Medline
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.
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