Tissue Specificity: Store-Operated Ca(2+) Entry in Cardiac Myocytes.

Tissue Specificity: Store-Operated Ca(2+) Entry in Cardiac Myocytes. Adv Exp Med Biol. 2017;993:363-387 Authors: Bootman MD, Rietdorf K Abstract Calcium (Ca(2+)) is a key regulator of cardiomyocyte contraction. The Ca(2+) channels, pumps, and exchangers responsible for the cyclical cytosolic Ca(2+) signals that underlie contraction are well known. In addition to those Ca(2+) signaling components responsible for contraction, it has been proposed that cardiomyocytes express channels that promote the influx of Ca(2+) from the extracellular milieu to the cytosol in response to depletion of intracellular Ca(2+) stores. With non-excitable cells, this store-operated Ca(2+) entry (SOCE) is usually easily demonstrated and is essential for prolonging cellular Ca(2+) signaling and for refilling depleted Ca(2+) stores. The role of SOCE in cardiomyocytes, however, is rather more elusive. While there is published evidence for increased Ca(2+) influx into cardiomyocytes following Ca(2+) 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 exp...
Source: Advances in Experimental Medicine and Biology - Category: Research Tags: Adv Exp Med Biol Source Type: research