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STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology.


Journal article


Helen E Collins, Xiaoyuan Zhu-Mauldin, R. Marchase, J. Chatham
American journal of physiology. Heart and circulatory physiology, 2013

Semantic Scholar DOI PubMed
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APA
Collins, H. E., Zhu-Mauldin, X., Marchase, R., & Chatham, J. (2013). STIM1/Orai1-mediated SOCE: current perspectives and potential roles in cardiac function and pathology. American Journal of Physiology. Heart and Circulatory Physiology.

Chicago/Turabian
Collins, Helen E, Xiaoyuan Zhu-Mauldin, R. Marchase, and J. Chatham. “STIM1/Orai1-Mediated SOCE: Current Perspectives and Potential Roles in Cardiac Function and Pathology.” American journal of physiology. Heart and circulatory physiology (2013).

MLA
Collins, Helen E., et al. “STIM1/Orai1-Mediated SOCE: Current Perspectives and Potential Roles in Cardiac Function and Pathology.” American Journal of Physiology. Heart and Circulatory Physiology, 2013.


Abstract

Store-operated Ca²⁺ entry (SOCE) is critical for Ca²⁺ signaling in nonexcitable cells; however, its role in the regulation of cardiomyocyte Ca²⁺ homeostasis has only recently been investigated. The increased understanding of the role of stromal interaction molecule 1 (STIM1) in regulating SOCE combined with recent studies demonstrating the presence of STIM1 in cardiomyocytes provides support that this pathway co-exists in the heart with the more widely recognized Ca²⁺ handling pathways associated with excitation-contraction coupling. There is now substantial evidence that STIM1-mediated SOCE plays a key role in mediating cardiomyocyte hypertrophy, both in vitro and in vivo, and there is growing support for the contribution of SOCE to Ca²⁺ overload associated with ischemia/reperfusion injury. Here, we provide an overview of our current understanding of the molecular regulation of SOCE and discuss the evidence supporting the role of STIM1/Orai1-mediated SOCE in regulating cardiomyocyte function.


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