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      <subfield code="a">Samouillan, Valerie</subfield>
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      <subfield code="a">García Rodríguez, Jesús Eduardo</subfield>
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      <subfield code="a">Benitez Amaro, Aleyda</subfield>
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      <subfield code="a">La Chica Lhoëst, Maria Teresa</subfield>
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      <subfield code="a">Actis Dato, Virginia</subfield>
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      <subfield code="a">Guerra Ramos, José María</subfield>
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      <subfield code="a">Escolà-Gil, Joan Carles</subfield>
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      <subfield code="a">Chiabrando, Gustavo</subfield>
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      <subfield code="a">Enrich, Carlos</subfield>
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      <subfield code="a">Llorente-Cortes, Vicenta</subfield>
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      <subfield code="a">Universitat Autònoma de Barcelona</subfield>
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      <subfield code="a">The accumulation of lipids in cardiomyocytes contributes to cardiac dysfunction. The specific blockage of cardiomyocyte cholesteryl ester (CE) loading by antibodies (Abs) against the P3 sequence (Gly 1127 -Cys 1140) of the LRP1 receptor improves cardiac insulin sensitivity. The impact of anti-P3 Abs on high-fat diet (HFD)-induced cardiac extracellular matrix (ECM) biophysical alterations was analyzed. Both IrP (without Abs) and P3-immunized rabbits (with Abs) were randomized into groups fed either HFD or a standard chow diet. Cardiac lipids, proteins, and carbohydrates were characterized by Fourier transform infrared spectroscopy in the attenuated total reflectance mode. The hydric organization and physical structure were determined by differential scanning calorimetry. HFD increased the levels of esterified lipids, collagen, and α-helical structures and upregulated fibrosis, bound water, and ECM plasticization in the heart. The inhibitory effect of anti-P3 Abs on cardiac CE accumulation was sufficient to reduce the collagen-filled extracellular space, the level of fibrosis, and the amount of bound water but did not counteract ECM plasticization in the heart of hypercholesterolemic rabbits.</subfield>
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      <subfield code="a">Inhibitory Effects of LRP1-Based Immunotherapy on Cardiac Extracellular Matrix Biophysical Alterations Induced by Hypercholesterolemia</subfield>
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