Calcium signaling as a mediator of cell energy demand and a trigger to cell death
Calcium signaling is pivotal to a host of physiological pathways. A rise in calcium concentration almost invariably signals an increased cellular energy demand. Consistent with this, calcium signals mediate a number of pathways that together serve to balance energy supply and demand. In pathological...
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Veröffentlicht in: | Annals of the New York Academy of Sciences 2015-09, Vol.1350 (1), p.107-116 |
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creator | Bhosale, Gauri Sharpe, Jenny A. Sundier, Stephanie Y. Duchen, Michael R. |
description | Calcium signaling is pivotal to a host of physiological pathways. A rise in calcium concentration almost invariably signals an increased cellular energy demand. Consistent with this, calcium signals mediate a number of pathways that together serve to balance energy supply and demand. In pathological states, calcium signals can precipitate mitochondrial injury and cell death, especially when coupled to energy depletion and oxidative or nitrosative stress. This review explores the mechanisms that couple cell signaling pathways to metabolic regulation or to cell death. The significance of these pathways is exemplified by pathological case studies, such as those showing loss of mitochondrial calcium uptake 1 in patients and ischemia/reperfusion injury. |
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A rise in calcium concentration almost invariably signals an increased cellular energy demand. Consistent with this, calcium signals mediate a number of pathways that together serve to balance energy supply and demand. In pathological states, calcium signals can precipitate mitochondrial injury and cell death, especially when coupled to energy depletion and oxidative or nitrosative stress. This review explores the mechanisms that couple cell signaling pathways to metabolic regulation or to cell death. The significance of these pathways is exemplified by pathological case studies, such as those showing loss of mitochondrial calcium uptake 1 in patients and ischemia/reperfusion injury.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/nyas.12885</identifier><identifier>PMID: 26375864</identifier><identifier>CODEN: ANYAA9</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Animals ; Apoptosis ; Calcium ; Calcium Signaling ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - metabolism ; Cation Transport Proteins - genetics ; Cation Transport Proteins - metabolism ; Cell Death ; Energy Metabolism ; Humans ; ischemia/reperfusion injury ; MICU1 ; Mitochondria - metabolism ; Mitochondria - pathology ; mitochondrial calcium uptake ; Mitochondrial Membrane Transport Proteins - genetics ; Mitochondrial Membrane Transport Proteins - metabolism ; Mitochondrial Membranes - chemistry ; Mitochondrial Membranes - metabolism ; Mitochondrial Membranes - pathology ; mitochondrial permeability transition pore ; Mitochondrial Proteins - genetics ; Mitochondrial Proteins - metabolism ; Models, Biological ; Mutation ; Necrosis ; Original ; Permeability ; Phosphate Transport Proteins - genetics ; Phosphate Transport Proteins - metabolism ; Porosity</subject><ispartof>Annals of the New York Academy of Sciences, 2015-09, Vol.1350 (1), p.107-116</ispartof><rights>2015 The Authors. published by Wiley Periodicals Inc. on behalf of The New York Academy of Sciences.</rights><rights>2015 The Authors. 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N.Y. Acad. Sci</addtitle><description>Calcium signaling is pivotal to a host of physiological pathways. A rise in calcium concentration almost invariably signals an increased cellular energy demand. Consistent with this, calcium signals mediate a number of pathways that together serve to balance energy supply and demand. In pathological states, calcium signals can precipitate mitochondrial injury and cell death, especially when coupled to energy depletion and oxidative or nitrosative stress. This review explores the mechanisms that couple cell signaling pathways to metabolic regulation or to cell death. The significance of these pathways is exemplified by pathological case studies, such as those showing loss of mitochondrial calcium uptake 1 in patients and ischemia/reperfusion injury.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Calcium</subject><subject>Calcium Signaling</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Cation Transport Proteins - genetics</subject><subject>Cation Transport Proteins - metabolism</subject><subject>Cell Death</subject><subject>Energy Metabolism</subject><subject>Humans</subject><subject>ischemia/reperfusion injury</subject><subject>MICU1</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>mitochondrial calcium uptake</subject><subject>Mitochondrial Membrane Transport Proteins - genetics</subject><subject>Mitochondrial Membrane Transport Proteins - metabolism</subject><subject>Mitochondrial Membranes - chemistry</subject><subject>Mitochondrial Membranes - metabolism</subject><subject>Mitochondrial Membranes - pathology</subject><subject>mitochondrial permeability transition pore</subject><subject>Mitochondrial Proteins - genetics</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Models, Biological</subject><subject>Mutation</subject><subject>Necrosis</subject><subject>Original</subject><subject>Permeability</subject><subject>Phosphate Transport Proteins - genetics</subject><subject>Phosphate Transport Proteins - metabolism</subject><subject>Porosity</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAUhS1ERYfChgdAltggpBT_O9kglRF0KlVFlH821k3ipC5JXOwEOm9fz6QdAQssWV74u5-OfRB6QskhTevlsIZ4SFmey3toQbUoMqU4u48WhGid5QXj--hhjJeEJEjoB2ifKa5lrsQCvV9CV7mpx9G1A3RuaDFEDLi3tYPRB-wbXNmuw3awoV3j2vYw1Hi78Rhc29qARz8ztYXx4hHaa6CL9vHteYA-vX3zcbnKTt8dnyyPTrNKMSazWuQcai0AWKV0VaqmKnMmOW90wxWhqijykhRNJcFqSUkpGwmCE6UbAVYCP0CvZu_VVKa0lR3GAJ25Cq6HsDYenPn7ZnAXpvW_jChEIRVLgue3guB_TjaOpndx8w4YrJ-ioZryQiguSEKf_YNe-imk_9pSTEnKCpGoFzNVBR9jsM0uDCVm05TZNGW2TSX46Z_xd-hdNQmgM_DbdXb9H5U5-3b04U6azTMujvZ6NwPhh1E6ec2Xs2Nz_nX1ebV8_d2c8xutHa29</recordid><startdate>201509</startdate><enddate>201509</enddate><creator>Bhosale, Gauri</creator><creator>Sharpe, Jenny A.</creator><creator>Sundier, Stephanie Y.</creator><creator>Duchen, Michael R.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>BSCLL</scope><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201509</creationdate><title>Calcium signaling as a mediator of cell energy demand and a trigger to cell death</title><author>Bhosale, Gauri ; Sharpe, Jenny A. ; Sundier, Stephanie Y. ; Duchen, Michael R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6225-d483ad74aa2c67cb6fcb82533f7f36016998b09fc5ae7510b5f5a43067f4ae5a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Calcium</topic><topic>Calcium Signaling</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Cation Transport Proteins - genetics</topic><topic>Cation Transport Proteins - metabolism</topic><topic>Cell Death</topic><topic>Energy Metabolism</topic><topic>Humans</topic><topic>ischemia/reperfusion injury</topic><topic>MICU1</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - pathology</topic><topic>mitochondrial calcium uptake</topic><topic>Mitochondrial Membrane Transport Proteins - genetics</topic><topic>Mitochondrial Membrane Transport Proteins - metabolism</topic><topic>Mitochondrial Membranes - chemistry</topic><topic>Mitochondrial Membranes - metabolism</topic><topic>Mitochondrial Membranes - pathology</topic><topic>mitochondrial permeability transition pore</topic><topic>Mitochondrial Proteins - genetics</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Models, Biological</topic><topic>Mutation</topic><topic>Necrosis</topic><topic>Original</topic><topic>Permeability</topic><topic>Phosphate Transport Proteins - genetics</topic><topic>Phosphate Transport Proteins - metabolism</topic><topic>Porosity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bhosale, Gauri</creatorcontrib><creatorcontrib>Sharpe, Jenny A.</creatorcontrib><creatorcontrib>Sundier, Stephanie Y.</creatorcontrib><creatorcontrib>Duchen, Michael R.</creatorcontrib><collection>Istex</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Environment Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bhosale, Gauri</au><au>Sharpe, Jenny A.</au><au>Sundier, Stephanie Y.</au><au>Duchen, Michael R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcium signaling as a mediator of cell energy demand and a trigger to cell death</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann. 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subjects | Animals Apoptosis Calcium Calcium Signaling Calcium-Binding Proteins - genetics Calcium-Binding Proteins - metabolism Cation Transport Proteins - genetics Cation Transport Proteins - metabolism Cell Death Energy Metabolism Humans ischemia/reperfusion injury MICU1 Mitochondria - metabolism Mitochondria - pathology mitochondrial calcium uptake Mitochondrial Membrane Transport Proteins - genetics Mitochondrial Membrane Transport Proteins - metabolism Mitochondrial Membranes - chemistry Mitochondrial Membranes - metabolism Mitochondrial Membranes - pathology mitochondrial permeability transition pore Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism Models, Biological Mutation Necrosis Original Permeability Phosphate Transport Proteins - genetics Phosphate Transport Proteins - metabolism Porosity |
title | Calcium signaling as a mediator of cell energy demand and a trigger to cell death |
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