<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-04-29T12:24:08Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/5226" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/5226</identifier><datestamp>2024-09-27T08:19:28Z</datestamp><setSpec>com_20.500.12105_19604</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19605</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Evrard, Solene M.</subfield>
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      <subfield code="a">Lecce, Laura</subfield>
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      <subfield code="a">Michelis, Katherine C.</subfield>
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      <subfield code="a">Nomura-Kitabayashi, Aya</subfield>
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      <subfield code="a">Pandey, Gaurav</subfield>
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      <subfield code="a">Purushothaman, K-Raman</subfield>
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      <subfield code="a">d'Escamard, Valentina</subfield>
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      <subfield code="a">Li, Jennifer R.</subfield>
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      <subfield code="a">Benard, Ludovic</subfield>
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      <subfield code="a">Nabel, Elizabeth G.</subfield>
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      <subfield code="a">Hajjar, Roger</subfield>
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      <subfield code="a">Fuster, Valentin</subfield>
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      <subfield code="a">Kovacic, Jason C.</subfield>
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      <subfield code="c">2016</subfield>
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      <subfield code="a">Endothelial to mesenchymal transition (EndMT) plays a major role during development, and also contributes to several adult cardiovascular diseases. Importantly, mesenchymal cells including fibroblasts are prominent in atherosclerosis, with key functions including regulation of: inflammation, matrix and collagen production, and plaque structural integrity. However, little is known about the origins of atherosclerosis-associated fibroblasts. Here we show using endothelial-specific lineage-tracking that EndMT-derived fibroblast-like cells are common in atherosclerotic lesions, with EndMT-derived cells expressing a range of fibroblast-specific markers. In vitro modelling confirms that EndMT is driven by TGF-beta signalling, oxidative stress and hypoxia; all hallmarks of atherosclerosis. `Transitioning' cells are readily detected in human plaques co-expressing endothelial and fibroblast/mesenchymal proteins, indicative of EndMT. The extent of EndMT correlates with an unstable plaque phenotype, which appears driven by altered collagen-MMP production in EndMT-derived cells. We conclude that EndMT contributes to atherosclerotic patho-biology and is associated with complex plaques that may be related to clinical events.</subfield>
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      <subfield code="a">Nat Commun. 2016; 7:11853</subfield>
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      <subfield code="a">10.1038/ncomms11853</subfield>
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      <subfield code="a">2041-1723</subfield>
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      <subfield code="a">Nature Communications</subfield>
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      <subfield code="a">27340017</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/5226</subfield>
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      <subfield code="a">FIBROBLAST ACTIVATION PROTEIN</subfield>
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      <subfield code="a">MARROW-DERIVED CELLS</subfield>
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      <subfield code="a">Endothelial to mesenchymal transition is common in atherosclerotic lesions and is associated with plaque instability</subfield>
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