Impaired biosynthesis of highly unsaturated phosphatidylcholines: a hypothesis on the molecular etiology of some muscular dystrophies
A brief review of the literature concerning the synthesis of phosphatidylcholine and phosphatidylethanolamine in muscle suggests that the cytidine pathways are replaced by the recently proposed acyl-specific de novo and salvage glycerolphosphodiester pathways ( Infante, 1984) in fully differentiated...
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| Veröffentlicht in: | Journal of theoretical biology 1985-09, Vol.116 (1), p.65-88 |
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| creator | Infante, Juan P. |
| description | A brief review of the literature concerning the synthesis of phosphatidylcholine and phosphatidylethanolamine in muscle suggests that the cytidine pathways are replaced by the recently proposed acyl-specific
de novo and salvage glycerolphosphodiester pathways (
Infante, 1984) in fully differentiated muscle. An analysis of published data suggests an impaired synthesis of 4,7,10,13,16,19-docosahexaenoic phosphatidylcholine, at the level of
de novo sn-3-glycerolphosphorylcholine synthesis, as the primary defect in Duchenne and (
dy) murine muscular dystrophies. This phosphatidylcholine species is postulated to be required for optimum sarcoplasmic Ca
2+ transport activity. It is proposed that this impairment initiates the secondary series of events which lead to the observed pathology of these diseases. Based on some predictions of the hypothesis, potential diagnosis and treatments are suggested. |
| doi_str_mv | 10.1016/S0022-5193(85)80131-4 |
| format | Article |
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de novo and salvage glycerolphosphodiester pathways (
Infante, 1984) in fully differentiated muscle. An analysis of published data suggests an impaired synthesis of 4,7,10,13,16,19-docosahexaenoic phosphatidylcholine, at the level of
de novo sn-3-glycerolphosphorylcholine synthesis, as the primary defect in Duchenne and (
dy) murine muscular dystrophies. This phosphatidylcholine species is postulated to be required for optimum sarcoplasmic Ca
2+ transport activity. It is proposed that this impairment initiates the secondary series of events which lead to the observed pathology of these diseases. Based on some predictions of the hypothesis, potential diagnosis and treatments are suggested.</description><identifier>ISSN: 0022-5193</identifier><identifier>EISSN: 1095-8541</identifier><identifier>DOI: 10.1016/S0022-5193(85)80131-4</identifier><identifier>PMID: 4046616</identifier><identifier>CODEN: JTBIAP</identifier><language>eng</language><publisher>Sidcup: Elsevier Ltd</publisher><subject>Animals ; Biological and medical sciences ; Calcium - metabolism ; Cell Differentiation ; Cells, Cultured ; Diseases of striated muscles. Neuromuscular diseases ; Glycerylphosphorylcholine - metabolism ; Humans ; Medical sciences ; Mice ; Muscles - metabolism ; Muscular Dystrophies - diagnosis ; Muscular Dystrophies - metabolism ; Muscular Dystrophies - therapy ; Muscular Dystrophy, Animal - metabolism ; Neurology ; Phosphatidylcholines - biosynthesis ; Phosphatidylethanolamines - biosynthesis ; Rats</subject><ispartof>Journal of theoretical biology, 1985-09, Vol.116 (1), p.65-88</ispartof><rights>1985 Academic Press Inc. (London) Ltd. All rights reserved</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-bb8474e7f4094d5e280548e49055c6cdf67ba44117bcb29b038e95a9bb3ac1e83</citedby><cites>FETCH-LOGICAL-c455t-bb8474e7f4094d5e280548e49055c6cdf67ba44117bcb29b038e95a9bb3ac1e83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0022-5193(85)80131-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8573763$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/4046616$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Infante, Juan P.</creatorcontrib><title>Impaired biosynthesis of highly unsaturated phosphatidylcholines: a hypothesis on the molecular etiology of some muscular dystrophies</title><title>Journal of theoretical biology</title><addtitle>J Theor Biol</addtitle><description>A brief review of the literature concerning the synthesis of phosphatidylcholine and phosphatidylethanolamine in muscle suggests that the cytidine pathways are replaced by the recently proposed acyl-specific
de novo and salvage glycerolphosphodiester pathways (
Infante, 1984) in fully differentiated muscle. An analysis of published data suggests an impaired synthesis of 4,7,10,13,16,19-docosahexaenoic phosphatidylcholine, at the level of
de novo sn-3-glycerolphosphorylcholine synthesis, as the primary defect in Duchenne and (
dy) murine muscular dystrophies. This phosphatidylcholine species is postulated to be required for optimum sarcoplasmic Ca
2+ transport activity. It is proposed that this impairment initiates the secondary series of events which lead to the observed pathology of these diseases. Based on some predictions of the hypothesis, potential diagnosis and treatments are suggested.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - metabolism</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Diseases of striated muscles. Neuromuscular diseases</subject><subject>Glycerylphosphorylcholine - metabolism</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Muscles - metabolism</subject><subject>Muscular Dystrophies - diagnosis</subject><subject>Muscular Dystrophies - metabolism</subject><subject>Muscular Dystrophies - therapy</subject><subject>Muscular Dystrophy, Animal - metabolism</subject><subject>Neurology</subject><subject>Phosphatidylcholines - biosynthesis</subject><subject>Phosphatidylethanolamines - biosynthesis</subject><subject>Rats</subject><issn>0022-5193</issn><issn>1095-8541</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhi1EVZbCI1TKASE4pNiJnThcKlQBrVSpB-Bs2c6kMXLi4HGQ8gC8N97usldOtvR_M575TMglo1eMsubDN0qrqhSsq99J8V5SVrOSPyM7RjtRSsHZc7I7IS_IS8SflNKO1805OeeUNw1rduTP3bRoF6EvjAu4zWkEdFiEoRjd4-i3Yp1RpzXqlJFlDLiMOrl-83YM3s2AHwtdjNsS_hXORb4VU_BgV69jAckFHx63fUsMU45WPCT9himGZXSAr8jZoD3C6-N5QX58-fz95ra8f_h6d_PpvrRciFQaI3nLoR143qMXUEkquATeUSFsY_uhaY3mnLHWWFN1htYSOqE7Y2ptGcj6grw99F1i-LUCJjU5tOC9niGsqNqm7qqWdhkUB9DGgBhhUEt0k46bYlTt9asn_WrvVkmhnvQrnusujw-sZoL-VHX0nfM3x1yj1X6IerYOT5gUbZ1nyNj1AYMs47eDqNA6mC30-atsUn1w_xnkL0oQpUg</recordid><startdate>19850907</startdate><enddate>19850907</enddate><creator>Infante, Juan P.</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</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>19850907</creationdate><title>Impaired biosynthesis of highly unsaturated phosphatidylcholines: a hypothesis on the molecular etiology of some muscular dystrophies</title><author>Infante, Juan P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-bb8474e7f4094d5e280548e49055c6cdf67ba44117bcb29b038e95a9bb3ac1e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - metabolism</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>Diseases of striated muscles. Neuromuscular diseases</topic><topic>Glycerylphosphorylcholine - metabolism</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Muscles - metabolism</topic><topic>Muscular Dystrophies - diagnosis</topic><topic>Muscular Dystrophies - metabolism</topic><topic>Muscular Dystrophies - therapy</topic><topic>Muscular Dystrophy, Animal - metabolism</topic><topic>Neurology</topic><topic>Phosphatidylcholines - biosynthesis</topic><topic>Phosphatidylethanolamines - biosynthesis</topic><topic>Rats</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Infante, Juan P.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of theoretical biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Infante, Juan P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impaired biosynthesis of highly unsaturated phosphatidylcholines: a hypothesis on the molecular etiology of some muscular dystrophies</atitle><jtitle>Journal of theoretical biology</jtitle><addtitle>J Theor Biol</addtitle><date>1985-09-07</date><risdate>1985</risdate><volume>116</volume><issue>1</issue><spage>65</spage><epage>88</epage><pages>65-88</pages><issn>0022-5193</issn><eissn>1095-8541</eissn><coden>JTBIAP</coden><abstract>A brief review of the literature concerning the synthesis of phosphatidylcholine and phosphatidylethanolamine in muscle suggests that the cytidine pathways are replaced by the recently proposed acyl-specific
de novo and salvage glycerolphosphodiester pathways (
Infante, 1984) in fully differentiated muscle. An analysis of published data suggests an impaired synthesis of 4,7,10,13,16,19-docosahexaenoic phosphatidylcholine, at the level of
de novo sn-3-glycerolphosphorylcholine synthesis, as the primary defect in Duchenne and (
dy) murine muscular dystrophies. This phosphatidylcholine species is postulated to be required for optimum sarcoplasmic Ca
2+ transport activity. It is proposed that this impairment initiates the secondary series of events which lead to the observed pathology of these diseases. Based on some predictions of the hypothesis, potential diagnosis and treatments are suggested.</abstract><cop>Sidcup</cop><pub>Elsevier Ltd</pub><pmid>4046616</pmid><doi>10.1016/S0022-5193(85)80131-4</doi><tpages>24</tpages></addata></record> |
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| source | Elsevier ScienceDirect Journals Complete - AutoHoldings; MEDLINE |
| subjects | Animals Biological and medical sciences Calcium - metabolism Cell Differentiation Cells, Cultured Diseases of striated muscles. Neuromuscular diseases Glycerylphosphorylcholine - metabolism Humans Medical sciences Mice Muscles - metabolism Muscular Dystrophies - diagnosis Muscular Dystrophies - metabolism Muscular Dystrophies - therapy Muscular Dystrophy, Animal - metabolism Neurology Phosphatidylcholines - biosynthesis Phosphatidylethanolamines - biosynthesis Rats |
| title | Impaired biosynthesis of highly unsaturated phosphatidylcholines: a hypothesis on the molecular etiology of some muscular dystrophies |
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