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Tissue Specificity: Store-Operated Ca2+ Entry in Cardiac Myocytes

Bootman, Martin D. and Rietdorf, Katja (2017). Tissue Specificity: Store-Operated Ca2+ Entry in Cardiac Myocytes. In: Groschner, K.; Graier, W. and Romanin, C. eds. Store-Operated Ca²⁺ Entry (SOCE) Pathways. Advances in Experimental Medicine and Biology, 993. Springer, pp. 363–387.

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Calcium (Ca2+) is a key regulator of cardiomyocyte contraction. The Ca2+ channels, pumps, and exchangers responsible for the cyclical cytosolic Ca2+ signals that underlie contraction are well known. In addition to those Ca2+ signaling components responsible for contraction, it has been proposed that cardiomyocytes express channels that promote the influx of Ca2+ from the extracellular milieu to the cytosol in response to depletion of intracellular Ca2+ stores. With non-excitable cells, this store-operated Ca2+ entry (SOCE) is usually easily demonstrated and is essential for prolonging cellular Ca2+ signaling and for refilling depleted Ca2+ stores. The role of SOCE in cardiomyocytes, however, is rather more elusive. While there is published evidence for increased Ca2+ influx into cardiomyocytes following Ca2+ store depletion, it has not been universally observed. Moreover, SOCE appears to be prominent in embryonic cardiomyocytes but declines with postnatal development. In contrast, there is overwhelming evidence that the molecular components of SOCE (e.g., STIM, Orai, and TRPC proteins) are expressed in cardiomyocytes from embryo to adult. Moreover, these proteins have been shown to contribute to disease conditions such as pathological hypertrophy, and reducing their expression can attenuate hypertrophic growth. It is plausible that SOCE might underlie Ca2+ influx into cardiomyocytes and may have important signaling functions perhaps by activating local Ca2+-sensitive processes. However, the STIM, Orai, and TRPC proteins appear to cooperate with multiple protein partners in signaling complexes. It is therefore possible that some of their signaling activities are not mediated by Ca2+ influx signals, but by protein-protein interactions.

Item Type: Book Section
Copyright Holders: 2017 Springer International Publishing AG
ISBN: 3-319-57732-8, 978-3-319-57732-6
ISSN: 0065-2598
Keywords: SOCE; Calcium; Signaling; Cardiac; Hypertrophy; Arrhythmia; Stromal interaction molecule; STIM
Academic Unit/School: Faculty of Science, Technology, Engineering and Mathematics (STEM) > Life, Health and Chemical Sciences
Faculty of Science, Technology, Engineering and Mathematics (STEM)
Research Group: Health and Wellbeing PRA (Priority Research Area)
Item ID: 50970
Depositing User: Martin Bootman
Date Deposited: 27 Sep 2017 10:22
Last Modified: 08 Dec 2018 13:38
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