Mitochondrial nitric oxide synthase: A masterpiece of metabolic adaptation, cell growth, transformation, and death
Mitochondria are specialized organelles that control energy metabolism and also activate a multiplicity of pathways that modulate cell proliferation and mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell death by a limited number of oxidative or nitrative reactions. Nit...
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| Veröffentlicht in: | Experimental biology and medicine (Maywood, N.J.) N.J.), 2009-09, Vol.234 (9), p.1020-1028 |
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| container_issue | 9 |
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| container_title | Experimental biology and medicine (Maywood, N.J.) |
| container_volume | 234 |
| creator | Finocchietto, Paola V Franco, Maria C Holod, Silvia Gonzalez, Analia S Converso, Daniela P Antico Arciuch, Valeria G Serra, Maria P Poderoso, Juan J Carreras, Maria C |
| description | Mitochondria are specialized organelles that control energy metabolism and also
activate a multiplicity of pathways that modulate cell proliferation and
mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell
death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO)
regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the
production of superoxide anion from the mitochondrial electron transfer chain. In
this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to
oxidation-reduction reaction (redox)–dependent cell signaling. Modulation of
translocation and activation of neuronal nitric oxide synthase (mtNOS activity) under
different physiologic or pathologic conditions represents an adaptive response
properly modulated to adjust mitochondria to different cell challenges. |
| doi_str_mv | 10.3181/0902-MR-81 |
| format | Article |
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activate a multiplicity of pathways that modulate cell proliferation and
mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell
death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO)
regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the
production of superoxide anion from the mitochondrial electron transfer chain. In
this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to
oxidation-reduction reaction (redox)–dependent cell signaling. Modulation of
translocation and activation of neuronal nitric oxide synthase (mtNOS activity) under
different physiologic or pathologic conditions represents an adaptive response
properly modulated to adjust mitochondria to different cell challenges.</description><identifier>ISSN: 1535-3699</identifier><identifier>ISSN: 1535-3702</identifier><identifier>EISSN: 1535-3699</identifier><identifier>DOI: 10.3181/0902-MR-81</identifier><identifier>PMID: 19546350</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>biochemical pathways ; cell growth ; Energy Metabolism ; insulin ; literature reviews ; mitochondria ; Mitochondria - enzymology ; Mitochondria - physiology ; nitric oxide ; Nitric Oxide - metabolism ; nitric oxide synthase ; Nitric Oxide Synthase - metabolism ; redox reactions ; signal transduction ; Stress, Physiological ; thyroid hormones</subject><ispartof>Experimental biology and medicine (Maywood, N.J.), 2009-09, Vol.234 (9), p.1020-1028</ispartof><rights>Copyright 2009 by the Society for Experimental Biology and Medicine</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c407t-6b2d9067826c5aa69ec3473e9f3c249546bc4617596ac9a03ea42876f1a883a13</citedby><cites>FETCH-LOGICAL-c407t-6b2d9067826c5aa69ec3473e9f3c249546bc4617596ac9a03ea42876f1a883a13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19546350$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Finocchietto, Paola V</creatorcontrib><creatorcontrib>Franco, Maria C</creatorcontrib><creatorcontrib>Holod, Silvia</creatorcontrib><creatorcontrib>Gonzalez, Analia S</creatorcontrib><creatorcontrib>Converso, Daniela P</creatorcontrib><creatorcontrib>Antico Arciuch, Valeria G</creatorcontrib><creatorcontrib>Serra, Maria P</creatorcontrib><creatorcontrib>Poderoso, Juan J</creatorcontrib><creatorcontrib>Carreras, Maria C</creatorcontrib><title>Mitochondrial nitric oxide synthase: A masterpiece of metabolic adaptation, cell growth, transformation, and death</title><title>Experimental biology and medicine (Maywood, N.J.)</title><addtitle>Exp Biol Med (Maywood)</addtitle><description>Mitochondria are specialized organelles that control energy metabolism and also
activate a multiplicity of pathways that modulate cell proliferation and
mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell
death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO)
regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the
production of superoxide anion from the mitochondrial electron transfer chain. In
this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to
oxidation-reduction reaction (redox)–dependent cell signaling. Modulation of
translocation and activation of neuronal nitric oxide synthase (mtNOS activity) under
different physiologic or pathologic conditions represents an adaptive response
properly modulated to adjust mitochondria to different cell challenges.</description><subject>biochemical pathways</subject><subject>cell growth</subject><subject>Energy Metabolism</subject><subject>insulin</subject><subject>literature reviews</subject><subject>mitochondria</subject><subject>Mitochondria - enzymology</subject><subject>Mitochondria - physiology</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>nitric oxide synthase</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>redox reactions</subject><subject>signal transduction</subject><subject>Stress, Physiological</subject><subject>thyroid hormones</subject><issn>1535-3699</issn><issn>1535-3702</issn><issn>1535-3699</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkE1LxDAQhoMofl_8AZqTglhNmjZNvIn4BS6CH-cwm053I22zJlnUf--WXdCDpxmYh4d5X0IOODsXXPELplmejZ4zxdfINi9FmQmp9fqffYvsxPjOGC-rXG6SLa7LQoqSbZMwcsnbqe_r4KClvUvBWeq_XI00fvdpChEv6RXtICYMM4cWqW9ohwnGvl2gUMMsQXK-P6MW25ZOgv9M0zOaAvSx8aFbHaGvaY2Qpntko4E24v5q7pK325vX6_vs8enu4frqMbMFq1Imx3mtmaxULm0JIDVaUVQCdSNsXgwBxraQvCq1BKuBCYQiV5VsOCglgItdcrz0zoL_mGNMpnNxeBF69PNoZCWZkkoswNMlaIOPMWBjZsF1EL4NZ2Zo2AwNm9GzUYP1cGWdjzusf9FVpQvgZAlEmKB59_PQL1L-rzpakg14A5Pgonl7yRkXjFe6VLoQP3uIjFc</recordid><startdate>20090901</startdate><enddate>20090901</enddate><creator>Finocchietto, Paola V</creator><creator>Franco, Maria C</creator><creator>Holod, Silvia</creator><creator>Gonzalez, Analia S</creator><creator>Converso, Daniela P</creator><creator>Antico Arciuch, Valeria G</creator><creator>Serra, Maria P</creator><creator>Poderoso, Juan J</creator><creator>Carreras, Maria C</creator><general>SAGE Publications</general><scope>FBQ</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>7X8</scope></search><sort><creationdate>20090901</creationdate><title>Mitochondrial nitric oxide synthase: A masterpiece of metabolic adaptation, cell growth, transformation, and death</title><author>Finocchietto, Paola V ; 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activate a multiplicity of pathways that modulate cell proliferation and
mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell
death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO)
regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the
production of superoxide anion from the mitochondrial electron transfer chain. In
this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to
oxidation-reduction reaction (redox)–dependent cell signaling. Modulation of
translocation and activation of neuronal nitric oxide synthase (mtNOS activity) under
different physiologic or pathologic conditions represents an adaptive response
properly modulated to adjust mitochondria to different cell challenges.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>19546350</pmid><doi>10.3181/0902-MR-81</doi><tpages>9</tpages></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | biochemical pathways cell growth Energy Metabolism insulin literature reviews mitochondria Mitochondria - enzymology Mitochondria - physiology nitric oxide Nitric Oxide - metabolism nitric oxide synthase Nitric Oxide Synthase - metabolism redox reactions signal transduction Stress, Physiological thyroid hormones |
| title | Mitochondrial nitric oxide synthase: A masterpiece of metabolic adaptation, cell growth, transformation, and death |
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