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BMB Rep. 2014 Feb;47(2):69-79.

Store-operated Ca2+ entry in muscle physiology and diseases.

Author information

1
Department of Internal Medicine-Cardiovascular Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
2
Muscle Biology Research Group-MUBIG, Schools of Nursing & Medicine, University of Missouri-Kansas City, MO, USA.
3
Department of Surgery, The Ohio State University Wexner Medical Center, Columbus, OH, USA; Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, USA.

Abstract

Ca(2+) release from intracellular stores and influx from extracellular reservoir regulate a wide range of physiological functions including muscle contraction and rhythmic heartbeat. One of the most ubiquitous pathways involved in controlled Ca(2+) influx into cells is store-operated Ca(2+) entry (SOCE), which is activated by the reduction of Ca(2+) concentration in the lumen of endoplasmic or sarcoplasmic reticulum (ER/SR). Although SOCE is pronounced in non-excitable cells, accumulating evidences highlight its presence and important roles in skeletal muscle and heart. Recent discovery of STIM proteins as ER/SR Ca(2+) sensors and Orai proteins as Ca(2+) channel pore forming unit expedited the mechanistic understanding of this pathway. This review focuses on current advances of SOCE components, regulation and physiologic and pathophysiologic roles in muscles. The specific property and the dysfunction of this pathway in muscle diseases, and new directions for future research in this rapidly growing field are discussed.

PMID:
24411466
PMCID:
PMC3967412
DOI:
10.5483/bmbrep.2014.47.2.015
[Indexed for MEDLINE]
Free PMC Article

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