<?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>2026-06-27T15:23:20Z</responseDate><request verb="GetRecord" identifier="oai:docta.ucm.es:20.500.14352/6445" metadataPrefix="marc">https://docta.ucm.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:docta.ucm.es:20.500.14352/6445</identifier><datestamp>2024-11-06T13:43:57Z</datestamp><setSpec>com_20.500.14352_14</setSpec><setSpec>col_20.500.14352_15</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Jiménez González, Sara</subfield>
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      <subfield code="a">Romero Miranda, Ana</subfield>
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      <subfield code="a">Luaces Méndez, María</subfield>
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      <subfield code="a">Islas, Fabián</subfield>
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      <subfield code="a">Nieto, María Luisa</subfield>
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      <subfield code="a">Martínez Martínez, Ernesto</subfield>
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      <subfield code="a">Cachofeiro Ramos, María Victoria</subfield>
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      <subfield code="a">The impact of the mitochondria-targeted antioxidant MitoQ was evaluated in the cardiac alterations associated with obesity. Male Wistar rats were fed either a high fat diet (HFD, 35% fat) or a standard diet (CT, 3.5% fat) for 7 weeks and treated with MitoQ (200 µM). The effect of MitoQ (5 nM) in rat cardiac myoblasts treated for 24 h with palmitic acid (PA, 200 µM) was evaluated. MitoQ reduced cardiac oxidative stress and prevented the development of cardiac fibrosis, hypertrophy, myocardial 18-FDG uptake reduction, and mitochondrial lipid remodeling in HFD rats. It also ameliorated cardiac mitochondrial protein level changes observed in HFD: reductions in fumarate hydratase, complex I and II, as well as increases in mitofusin 1 (MFN1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha, and cyclophilin F (cycloF). In vitro, MitoQ prevented oxidative stress and ameliorated alterations in mitochondrial proteins observed in palmitic acid (PA)-stimulated cardiac myoblasts: increases in carnitine palmitoyltransferase 1A, cycloF, and cytochrome C. PA induced phosphorylation of extracellular signal-regulated kinases and nuclear factor-κB p65. Therefore, the data show the beneficial effects of MitoQ in the cardiac damage induced by obesity and suggests a crosstalk between lipotoxicity and mitochondrial oxidative stress in this damage.</subfield>
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      <subfield code="a">2073-4409</subfield>
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      <subfield code="a">10.3390/cells9020451</subfield>
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      <subfield code="a">https://hdl.handle.net/20.500.14352/6445</subfield>
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      <subfield code="a">https://www.mdpi.com/2073-4409/9/2/451</subfield>
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      <subfield code="a">The Crosstalk between Cardiac Lipotoxicity and Mitochondrial Oxidative Stress in the Cardiac Alterations in Diet-Induced Obesity in Rats</subfield>
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