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Life after the birth of the mitochondrial Na^＋/Ca^2＋ exchanger,NCLX
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Life after the birth of the mitochondrial Na^＋/Ca^2＋ exchanger,NCLX
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Life after the birth of the mitochondrial Na^＋/Ca^2＋ exchanger,NCLX
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Journal Article
Life after the birth of the mitochondrial Na^＋/Ca^2＋ exchanger,NCLX
2015
Overview
Powered by the mitochondrial membrane potential,Ca^2＋ permeates the mitochondria via a Ca^2＋ channel termed Ca^2＋ uniporter and is pumped out by a Na＋/Ca^2＋ exchanger,both of which are located on the inner mitochondrial membrane.Mitochondrial Ca^2＋ transients are critical for metabolic activity and regulating global Ca^2＋ responses.On the other hand,failure to control mitochondrial Ca^2＋ is a hallmark of ischemic and neurodegenerative diseases.Despite their importance,identifying the uniporter and exchanger remains elusive and their inhibitors are non-specific.This review will focus on the mitochondrial exchanger,initially describing how it was molecularly identified and linked to a novel member of the Na^＋/Ca^2＋ exchanger superfamily termed NCLX.Molecular control of NCLX expression provides a selective tool to determine its physiological role in a variety of cell types.In lymphocytes,NCLX is essential for refilling the endoplasmic reticulum Ca^2＋ stores required for antigen-dependent signaling.Communication of NCLX with the store-operated channel in astroglia controls Ca^2＋ influx and thereby neuro-transmitter release and cell proliferation.The refilling of the Ca^2＋ stores in the sarcoplasmic reticulum,which is controlled by NCLX,determines the frequency of action potential and Ca^2＋ transients in cardiomyocytes.NCLX is emerging as a hub for integrating glucose-dependent Na＋ and Ca^2＋ signaling in pancreatic β cells,and the specific molecular control of NCLX expression resolved the controversy regarding its role in neurons and β cells.Future studies on an NCLX knockdown mouse model and identification of human NCLX mutations are expected to determine the role of mitochondrial Ca^2＋ efflux in organ activity and whether NCLX inactivation is linked to ischemic and/or neurodegenerative syndromes.Structure-function analysis and protein analysis will identify the NCLX mode of regulation and its partners in the inner membrane of the mitochondria.
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