LYMPHATIC VESSEL INSUFFICIENCY IN HYPERCHOLESTEROLEMIC MICE ALTERS LIPOPROTEIN LEVELS AND PROMOTES ATHEROGENESIS
Identifieur interne : 003A32 ( Pmc/Corpus ); précédent : 003A31; suivant : 003A33LYMPHATIC VESSEL INSUFFICIENCY IN HYPERCHOLESTEROLEMIC MICE ALTERS LIPOPROTEIN LEVELS AND PROMOTES ATHEROGENESIS
Auteurs : Taina Vuorio ; Harri Nurmi ; Karen Moulton ; Jere Pikkarainen ; Marius R. Robciuc ; Miina Öhman ; Suvi E. Heinonen ; Haritha Samaranayake ; Tommi Heikura ; Kari Alitalo ; Seppo Yl HerttualaSource :
- Arteriosclerosis, thrombosis, and vascular biology [ 1079-5642 ] ; 2014.
Abstract
Lymphatic vessels collect extravasated fluid and proteins from tissues to blood circulation as well as play an essential role in lipid metabolism by taking up intestinal chylomicrons. Previous studies have shown that impairment of lymphatic vessel function causes lymphedema and fat accumulation, but clear connections between arterial pathologies and lymphatic vessels have not been described.
Two transgenic mouse strains with lymphatic insufficiency (sVEGFR3 and Chy) were crossed with atherosclerotic mice (LDLR−/−/ApoB100/100) to study the effects of insufficient lymphatic vessel transport on lipoprotein metabolism and atherosclerosis. Both sVEGFR3 × LDLR−/−/ApoB100/100 mice and Chy × LDLR−/−/ApoB100/100 mice had higher plasma cholesterol levels compared to LDLR−/−/ApoB100/100 control mice during both normal chow diet (16.3 mmol/l and 13.7 mmol/l vs. 8.2 mmol/l, respectively) and Western-type high fat diet (e.g. after 2 weeks of fat diet 45.9 mmol/l and 42.6 mmol/l vs. 30.2 mmol/l, respectively). Cholesterol and triglyceride levels in very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) fractions were increased. Atherosclerotic lesions in young and intermediate cohorts of sVEGFR3 × LDLR−/−/ApoB100/100 mice progressed faster than in control mice (e.g. intermediate cohort mice at 6 weeks 18.3% vs. 7.7% of the whole aorta, respectively). In addition, lesions in sVEGFR3 × LDLR−/−/ApoB100/100 mice and Chy × LDLR−/−/ApoB100/100 mice had much less lymphatic vessels than lesions in control mice (0.33% and 1.07% vs. 7.45% of podoplanin positive vessels, respectively).
We show a novel finding linking impaired lymphatic vessels to lipoprotein metabolism, increased plasma cholesterol levels and enhanced atherogenesis.
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DOI: 10.1161/ATVBAHA.114.302528
PubMed: 24723556
PubMed Central: 4031366
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">LYMPHATIC VESSEL INSUFFICIENCY IN HYPERCHOLESTEROLEMIC MICE ALTERS LIPOPROTEIN LEVELS AND PROMOTES ATHEROGENESIS</title><author><name sortKey="Vuorio, Taina" sort="Vuorio, Taina" uniqKey="Vuorio T" first="Taina" last="Vuorio">Taina Vuorio</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Nurmi, Harri" sort="Nurmi, Harri" uniqKey="Nurmi H" first="Harri" last="Nurmi">Harri Nurmi</name><affiliation><nlm:aff id="A2">Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</nlm:aff></affiliation></author><author><name sortKey="Moulton, Karen" sort="Moulton, Karen" uniqKey="Moulton K" first="Karen" last="Moulton">Karen Moulton</name><affiliation><nlm:aff id="A3">Cardiology Division, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA</nlm:aff></affiliation></author><author><name sortKey="Pikkarainen, Jere" sort="Pikkarainen, Jere" uniqKey="Pikkarainen J" first="Jere" last="Pikkarainen">Jere Pikkarainen</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Robciuc, Marius R" sort="Robciuc, Marius R" uniqKey="Robciuc M" first="Marius R." last="Robciuc">Marius R. Robciuc</name><affiliation><nlm:aff id="A2">Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</nlm:aff></affiliation></author><author><name sortKey="Ohman, Miina" sort="Ohman, Miina" uniqKey="Ohman M" first="Miina" last="Öhman">Miina Öhman</name><affiliation><nlm:aff id="A2">Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</nlm:aff></affiliation></author><author><name sortKey="Heinonen, Suvi E" sort="Heinonen, Suvi E" uniqKey="Heinonen S" first="Suvi E." last="Heinonen">Suvi E. Heinonen</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Samaranayake, Haritha" sort="Samaranayake, Haritha" uniqKey="Samaranayake H" first="Haritha" last="Samaranayake">Haritha Samaranayake</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Heikura, Tommi" sort="Heikura, Tommi" uniqKey="Heikura T" first="Tommi" last="Heikura">Tommi Heikura</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name><affiliation><nlm:aff id="A2">Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</nlm:aff></affiliation></author><author><name sortKey="Yl Herttuala, Seppo" sort="Yl Herttuala, Seppo" uniqKey="Yl Herttuala S" first="Seppo" last="Yl Herttuala">Seppo Yl Herttuala</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation><affiliation><nlm:aff id="A4">Gene Therapy Unit, Kuopio University Hospital, P.O. Box 1777, FI-70211 Kuopio, Finland</nlm:aff></affiliation><affiliation><nlm:aff id="A5">Research Unit, Kuopio University Hospital, P.O. Box 1777, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24723556</idno><idno type="pmc">4031366</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031366</idno><idno type="RBID">PMC:4031366</idno><idno type="doi">10.1161/ATVBAHA.114.302528</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">003A32</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003A32</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">LYMPHATIC VESSEL INSUFFICIENCY IN HYPERCHOLESTEROLEMIC MICE ALTERS LIPOPROTEIN LEVELS AND PROMOTES ATHEROGENESIS</title><author><name sortKey="Vuorio, Taina" sort="Vuorio, Taina" uniqKey="Vuorio T" first="Taina" last="Vuorio">Taina Vuorio</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Nurmi, Harri" sort="Nurmi, Harri" uniqKey="Nurmi H" first="Harri" last="Nurmi">Harri Nurmi</name><affiliation><nlm:aff id="A2">Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</nlm:aff></affiliation></author><author><name sortKey="Moulton, Karen" sort="Moulton, Karen" uniqKey="Moulton K" first="Karen" last="Moulton">Karen Moulton</name><affiliation><nlm:aff id="A3">Cardiology Division, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA</nlm:aff></affiliation></author><author><name sortKey="Pikkarainen, Jere" sort="Pikkarainen, Jere" uniqKey="Pikkarainen J" first="Jere" last="Pikkarainen">Jere Pikkarainen</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Robciuc, Marius R" sort="Robciuc, Marius R" uniqKey="Robciuc M" first="Marius R." last="Robciuc">Marius R. Robciuc</name><affiliation><nlm:aff id="A2">Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</nlm:aff></affiliation></author><author><name sortKey="Ohman, Miina" sort="Ohman, Miina" uniqKey="Ohman M" first="Miina" last="Öhman">Miina Öhman</name><affiliation><nlm:aff id="A2">Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</nlm:aff></affiliation></author><author><name sortKey="Heinonen, Suvi E" sort="Heinonen, Suvi E" uniqKey="Heinonen S" first="Suvi E." last="Heinonen">Suvi E. Heinonen</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Samaranayake, Haritha" sort="Samaranayake, Haritha" uniqKey="Samaranayake H" first="Haritha" last="Samaranayake">Haritha Samaranayake</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Heikura, Tommi" sort="Heikura, Tommi" uniqKey="Heikura T" first="Tommi" last="Heikura">Tommi Heikura</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author><author><name sortKey="Alitalo, Kari" sort="Alitalo, Kari" uniqKey="Alitalo K" first="Kari" last="Alitalo">Kari Alitalo</name><affiliation><nlm:aff id="A2">Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</nlm:aff></affiliation></author><author><name sortKey="Yl Herttuala, Seppo" sort="Yl Herttuala, Seppo" uniqKey="Yl Herttuala S" first="Seppo" last="Yl Herttuala">Seppo Yl Herttuala</name><affiliation><nlm:aff id="A1">A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</nlm:aff></affiliation><affiliation><nlm:aff id="A4">Gene Therapy Unit, Kuopio University Hospital, P.O. Box 1777, FI-70211 Kuopio, Finland</nlm:aff></affiliation><affiliation><nlm:aff id="A5">Research Unit, Kuopio University Hospital, P.O. Box 1777, FI-70211 Kuopio, Finland</nlm:aff></affiliation></author></analytic><series><title level="j">Arteriosclerosis, thrombosis, and vascular biology</title><idno type="ISSN">1079-5642</idno><idno type="eISSN">1524-4636</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Objective</title><p id="P1">Lymphatic vessels collect extravasated fluid and proteins from tissues to blood circulation as well as play an essential role in lipid metabolism by taking up intestinal chylomicrons. Previous studies have shown that impairment of lymphatic vessel function causes lymphedema and fat accumulation, but clear connections between arterial pathologies and lymphatic vessels have not been described.</p></sec><sec id="S2"><title>Approach and Results</title><p id="P2">Two transgenic mouse strains with lymphatic insufficiency (sVEGFR3 and Chy) were crossed with atherosclerotic mice (LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup>) to study the effects of insufficient lymphatic vessel transport on lipoprotein metabolism and atherosclerosis. Both sVEGFR3 × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice and Chy × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice had higher plasma cholesterol levels compared to LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> control mice during both normal chow diet (16.3 mmol/l and 13.7 mmol/l vs. 8.2 mmol/l, respectively) and Western-type high fat diet (e.g. after 2 weeks of fat diet 45.9 mmol/l and 42.6 mmol/l vs. 30.2 mmol/l, respectively). Cholesterol and triglyceride levels in very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) fractions were increased. Atherosclerotic lesions in young and intermediate cohorts of sVEGFR3 × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice progressed faster than in control mice (e.g. intermediate cohort mice at 6 weeks 18.3% vs. 7.7% of the whole aorta, respectively). In addition, lesions in sVEGFR3 × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice and Chy × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice had much less lymphatic vessels than lesions in control mice (0.33% and 1.07% vs. 7.45% of podoplanin positive vessels, respectively).</p></sec><sec id="S3"><title>Conclusions</title><p id="P3">We show a novel finding linking impaired lymphatic vessels to lipoprotein metabolism, increased plasma cholesterol levels and enhanced atherogenesis.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9505803</journal-id><journal-id journal-id-type="pubmed-jr-id">8623</journal-id><journal-id journal-id-type="nlm-ta">Arterioscler Thromb Vasc Biol</journal-id><journal-id journal-id-type="iso-abbrev">Arterioscler. Thromb. Vasc. Biol.</journal-id><journal-title-group><journal-title>Arteriosclerosis, thrombosis, and vascular biology</journal-title></journal-title-group><issn pub-type="ppub">1079-5642</issn><issn pub-type="epub">1524-4636</issn></journal-meta><article-meta><article-id pub-id-type="pmid">24723556</article-id><article-id pub-id-type="pmc">4031366</article-id><article-id pub-id-type="doi">10.1161/ATVBAHA.114.302528</article-id><article-id pub-id-type="manuscript">NIHMS581451</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>LYMPHATIC VESSEL INSUFFICIENCY IN HYPERCHOLESTEROLEMIC MICE ALTERS LIPOPROTEIN LEVELS AND PROMOTES ATHEROGENESIS</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Vuorio</surname><given-names>Taina</given-names></name><degrees>MSc</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Nurmi</surname><given-names>Harri</given-names></name><degrees>MSc</degrees><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Moulton</surname><given-names>Karen</given-names></name><degrees>MD, PhD</degrees><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Pikkarainen</surname><given-names>Jere</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Robciuc</surname><given-names>Marius R.</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>öhman</surname><given-names>Miina</given-names></name><degrees>MD, PhD</degrees><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Heinonen</surname><given-names>Suvi E.</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Samaranayake</surname><given-names>Haritha</given-names></name><degrees>PhD</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Heikura</surname><given-names>Tommi</given-names></name><degrees>MSc</degrees><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Alitalo</surname><given-names>Kari</given-names></name><degrees>MD, PhD</degrees><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Ylä-Herttuala</surname><given-names>Seppo</given-names></name><degrees>MD, PhD, FESC</degrees><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A4">4</xref><xref ref-type="aff" rid="A5">5</xref></contrib></contrib-group><aff id="A1"><label>1</label>A.I. Virtanen Institute for Molecular Sciences, Department of Biotechnology and Molecular Medicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland</aff><aff id="A2"><label>2</label>Wihuri Research Institute and Translational Biology Program, Biomedicum Helsinki, Haartmaninkatu 8 (P.O. Box 63), FI-00014 University of Helsinki, Helsinki, Finland</aff><aff id="A3"><label>3</label>Cardiology Division, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA</aff><aff id="A4"><label>4</label>Gene Therapy Unit, Kuopio University Hospital, P.O. Box 1777, FI-70211 Kuopio, Finland</aff><aff id="A5"><label>5</label>Research Unit, Kuopio University Hospital, P.O. Box 1777, FI-70211 Kuopio, Finland</aff><author-notes><corresp id="CR1">Corresponding author: Seppo Ylä-Herttuala MD, PhD, FESC A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland P.O. Box 1627 FI-70211 Kuopio, Finland <email>Seppo.Ylaherttuala@uef.fi</email> Tel. +358 403552075</corresp></author-notes><pub-date pub-type="nihms-submitted"><day>16</day><month>5</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>10</day><month>4</month><year>2014</year></pub-date><pub-date pub-type="ppub"><month>6</month><year>2014</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>6</month><year>2015</year></pub-date><volume>34</volume><issue>6</issue><fpage>1162</fpage><lpage>1170</lpage><pmc-comment>elocation-id from pubmed: 10.1161/ATVBAHA.114.302528</pmc-comment>
<abstract><sec id="S1"><title>Objective</title><p id="P1">Lymphatic vessels collect extravasated fluid and proteins from tissues to blood circulation as well as play an essential role in lipid metabolism by taking up intestinal chylomicrons. Previous studies have shown that impairment of lymphatic vessel function causes lymphedema and fat accumulation, but clear connections between arterial pathologies and lymphatic vessels have not been described.</p></sec><sec id="S2"><title>Approach and Results</title><p id="P2">Two transgenic mouse strains with lymphatic insufficiency (sVEGFR3 and Chy) were crossed with atherosclerotic mice (LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup>) to study the effects of insufficient lymphatic vessel transport on lipoprotein metabolism and atherosclerosis. Both sVEGFR3 × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice and Chy × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice had higher plasma cholesterol levels compared to LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> control mice during both normal chow diet (16.3 mmol/l and 13.7 mmol/l vs. 8.2 mmol/l, respectively) and Western-type high fat diet (e.g. after 2 weeks of fat diet 45.9 mmol/l and 42.6 mmol/l vs. 30.2 mmol/l, respectively). Cholesterol and triglyceride levels in very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) fractions were increased. Atherosclerotic lesions in young and intermediate cohorts of sVEGFR3 × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice progressed faster than in control mice (e.g. intermediate cohort mice at 6 weeks 18.3% vs. 7.7% of the whole aorta, respectively). In addition, lesions in sVEGFR3 × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice and Chy × LDLR<sup>−/−</sup>/ApoB<sup>100/100</sup> mice had much less lymphatic vessels than lesions in control mice (0.33% and 1.07% vs. 7.45% of podoplanin positive vessels, respectively).</p></sec><sec id="S3"><title>Conclusions</title><p id="P3">We show a novel finding linking impaired lymphatic vessels to lipoprotein metabolism, increased plasma cholesterol levels and enhanced atherogenesis.</p></sec></abstract><kwd-group><kwd>Atherosclerosis</kwd><kwd>Lymphatic capillary</kwd><kwd>Lipoprotein</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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