STIM1/Orai1-mediated SOCE: Current Perspectives and Potential Roles in Cardiac Function and Pathology

Overview

Journal Am J Physiol Heart Circ Physiol

Publisher American Physiological Society

Specialties Cardiology & Vascular Diseases
Physiology

Date 2013 Jun 25

PMID 23792674

Citations 66

Authors

Helen E Collins

Xiaoyuan Zhu-Mauldin

Richard B Marchase

John C Chatham

Affiliations

Soon will be listed here.

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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