Mechanisms modulating foam cell formation in the arterial intima: exploring new therapeutic opportunities in atherosclerosis

Mostra el registre complet Registre parcial de l'ítem

• dc.contributor.author La Chica Lhoëst, María Teresa
• dc.contributor.author Martinez, A.
• dc.contributor.author Claudi, Lene
• dc.contributor.author Garcia, E.
• dc.contributor.author Benitez-Amaro, Aleyda
• dc.contributor.author Polishchuk, Anna
• dc.contributor.author Piñero González, Janet, 1977-
• dc.contributor.author Viladés-Medel, David
• dc.contributor.author Guerra, Jose M.
• dc.contributor.author Sanz, Ferran
• dc.contributor.author Rotllan, Noemí
• dc.contributor.author Escolà-Gil, Joan Carles
• dc.contributor.author Llorente-Cortés, Vicenta
• dc.date.accessioned 2025-03-28T07:11:55Z
• dc.date.available 2025-03-28T07:11:55Z
• dc.date.issued 2024
• dc.description.abstract In recent years, the role of macrophages as the primary cell type contributing to foam cell formation and atheroma plaque development has been widely acknowledged. However, it has been long recognized that diffuse intimal thickening (DIM), which precedes the formation of early fatty streaks in humans, primarily consists of lipid-loaded smooth muscle cells (SMCs) and their secreted proteoglycans. Recent studies have further supported the notion that SMCs constitute the majority of foam cells in advanced atherosclerotic plaques. Given that SMCs are a major component of the vascular wall, they serve as a significant source of microvesicles and exosomes, which have the potential to regulate the physiology of other vascular cells. Notably, more than half of the foam cells present in atherosclerotic lesions are of SMC origin. In this review, we describe several mechanisms underlying the formation of intimal foam-like cells in atherosclerotic plaques. Based on these mechanisms, we discuss novel therapeutic approaches that have been developed to regulate the generation of intimal foam-like cells. These innovative strategies hold promise for improving the management of atherosclerosis in the near future.
• dc.description.sponsorship The economic support to develop this project was received from FIS PI21/01523 (to VLl-C) from the Instituto de Salud Carlos III (ISCIII) and co-financed with ERDFs, and Fundación BBVA Ayudas a equipos de investigación 2019. Aleyda Benitez Amaro (ABA) is a postdoctoral fellow (FI19/00205) that was granted by the Programme Contratos predoctorales de formación de investigación en salud_from the Instituto de Salud Carlos III (ISCIII) and co-financed with ERDFs. The RIFS methodology required to analyze mitochondrial respiration in frozen cardiac samples was developed thanks to the AYUDAS PARA LA MOVILIDAD DE PERSONAL INVESTIGADOR CONTRATADO EN EL MARCO DE LA AES (M-AES) del ISCIII granted by ABA (MV21/00060). Our group is part of CIBER Enfermedades Cardiovasculares (CIBERCV; CB16/11/00276 to VLl-C), and CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM; CB07/08/016 to JC-EG and NR), projects run by the Instituto de Salud Carlos III. Our group also participates in Redes de investigación (Enfermedades Metabóloicas y Cáncer RED2018-102799-T), a project run by MINECO. We belong to a group recognized by Generalitat de Catalunya (2021 SGR 00834). This work was also funded by Ministerio de Ciencia, Innovación y Universidades (PID2022-137186OB-100), as well as from the Agencia Estatal de Investigación (AEI/10.13039/501100011033) within the Subprograma Ramón y Cajal (RYC-201722879) to NR. The IR SANT PAU is a centre of CERCA Programme/Generalitat de Catalunya
• dc.format.mimetype application/pdf
• dc.identifier.citation La Chica Lhoëst MT, Martinez A, Claudi L, Garcia E, Benitez-Amaro A, Polishchuk A, et al. Mechanisms modulating foam cell formation in the arterial intima: exploring new therapeutic opportunities in atherosclerosis. Front Cardiovasc Med. 2024 Jun 17;11:1381520. DOI: 10.3389/fcvm.2024.1381520
• dc.identifier.doi http://dx.doi.org/10.3389/fcvm.2024.1381520
• dc.identifier.issn 2297-055X
• dc.identifier.uri http://hdl.handle.net/10230/70039
• dc.language.iso eng
• dc.publisher Frontiers
• dc.relation.ispartof Front Cardiovasc Med. 2024 Jun 17;11:1381520
• dc.relation.projectID info:eu-repo/grantAgreement/ES/3PE/PID2022-137186OB-100
• dc.rights © 2024 La Chica Lhoëst, Martinez, Claudi, Garcia, Benitez-Amaro, Polishchuk, Piñero, Vilades, Guerra, Sanz, Rotllan, Escolà-Gil and Llorente-Cortés. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri http://creativecommons.org/licenses/by/4.0/
• dc.subject.keyword apoA1
• dc.subject.keyword apoC1
• dc.subject.keyword apoE)
• dc.subject.keyword apoJ
• dc.subject.keyword Apolipoproteins (ApoB100
• dc.subject.keyword Atherosclerosis
• dc.subject.keyword Cardiovascular diseases
• dc.subject.keyword Foam-like SMC
• dc.subject.keyword Lipoproteins
• dc.subject.keyword Peptidomimetics
• dc.subject.keyword Reverse cholesterol transport
• dc.subject.keyword Transcription factors
• dc.title Mechanisms modulating foam cell formation in the arterial intima: exploring new therapeutic opportunities in atherosclerosis
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion