Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer

Atherosclerotic arterial plaques and malignant solid tumors contain macrophages, which participate in anaerobic metabolism, acidosis, and inflammatory processes inherent in the development of either disease. The tissue-resident macrophage populations originate from precursor cells derived from the y...

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Autores: Lee-Rueckert, Miriam, Lappalainen, Jani, Kovanen, Petri T., Escolà-Gil, Joan Carles|||0000-0001-9021-2485
Tipo de recurso: artículo
Fecha de publicación:2022
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:282319
Acceso en línea:https://ddd.uab.cat/record/282319
https://dx.doi.org/urn:doi:10.3389/fcvm.2022.777822
Access Level:acceso abierto
Palabra clave:Atherosclerosis
Cancer
Inflammation
LDL
Macrophages
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spelling Lipid-Laden Macrophages and Inflammation in Atherosclerosis and CancerAn Integrative ViewLee-Rueckert, MiriamLappalainen, JaniKovanen, Petri T.Escolà-Gil, Joan Carles|||0000-0001-9021-2485AtherosclerosisCancerInflammationLDLMacrophagesAtherosclerotic arterial plaques and malignant solid tumors contain macrophages, which participate in anaerobic metabolism, acidosis, and inflammatory processes inherent in the development of either disease. The tissue-resident macrophage populations originate from precursor cells derived from the yolk sac and from circulating bone marrow-derived monocytes. In the tissues, they differentiate into varying functional phenotypes in response to local microenvironmental stimulation. Broadly categorized, the macrophages are activated to polarize into proinflammatory M1 and anti-inflammatory M2 phenotypes; yet, noticeable plasticity allows them to dynamically shift between several distinct functional subtypes. In atherosclerosis, low-density lipoprotein (LDL)-derived cholesterol accumulates within macrophages as cytoplasmic lipid droplets thereby generating macrophage foam cells, which are involved in all steps of atherosclerosis. The conversion of macrophages into foam cells may suppress the expression of given proinflammatory genes and thereby initiate their transcriptional reprogramming toward an anti-inflammatory phenotype. In this particular sense, foam cell formation can be considered anti-atherogenic. The tumor-associated macrophages (TAMs) may become polarized into anti-tumoral M1 and pro-tumoral M2 phenotypes. Mechanistically, the TAMs can regulate the survival and proliferation of the surrounding cancer cells and participate in various aspects of tumor formation, progression, and metastasis. The TAMs may accumulate lipids, but their type and their specific roles in tumorigenesis are still poorly understood. Here, we discuss how the phenotypic and functional plasticity of macrophages allows their multifunctional response to the distinct microenvironments in developing atherosclerotic lesions and in developing malignant tumors. We also discuss how the inflammatory reactions of the macrophages may influence the development of atherosclerotic plaques and malignant tumors, and highlight the potential therapeutic effects of targeting lipid-laden macrophages in either disease. 22022-01-0120222022-01-01Article de revisióhttp://purl.org/coar/resource_type/c_dcae04bcVoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://ddd.uab.cat/record/282319https://dx.doi.org/urn:doi:10.3389/fcvm.2022.777822reponame:Dipòsit Digital de Documents de la UABinstname:Universitat Autònoma de BarcelonaInglésengInstituto de Salud Carlos III https://doi.org/10.13039/501100004587 PI1900136open accesshttp://purl.org/coar/access_right/c_abf2Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:ddd.uab.cat:2823192026-06-06T12:50:31Z
dc.title.none.fl_str_mv Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer
An Integrative View
title Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer
spellingShingle Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer
Lee-Rueckert, Miriam
Atherosclerosis
Cancer
Inflammation
LDL
Macrophages
title_short Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer
title_full Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer
title_fullStr Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer
title_full_unstemmed Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer
title_sort Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer
dc.creator.none.fl_str_mv Lee-Rueckert, Miriam
Lappalainen, Jani
Kovanen, Petri T.
Escolà-Gil, Joan Carles|||0000-0001-9021-2485
author Lee-Rueckert, Miriam
author_facet Lee-Rueckert, Miriam
Lappalainen, Jani
Kovanen, Petri T.
Escolà-Gil, Joan Carles|||0000-0001-9021-2485
author_role author
author2 Lappalainen, Jani
Kovanen, Petri T.
Escolà-Gil, Joan Carles|||0000-0001-9021-2485
author2_role author
author
author
dc.subject.none.fl_str_mv Atherosclerosis
Cancer
Inflammation
LDL
Macrophages
topic Atherosclerosis
Cancer
Inflammation
LDL
Macrophages
description Atherosclerotic arterial plaques and malignant solid tumors contain macrophages, which participate in anaerobic metabolism, acidosis, and inflammatory processes inherent in the development of either disease. The tissue-resident macrophage populations originate from precursor cells derived from the yolk sac and from circulating bone marrow-derived monocytes. In the tissues, they differentiate into varying functional phenotypes in response to local microenvironmental stimulation. Broadly categorized, the macrophages are activated to polarize into proinflammatory M1 and anti-inflammatory M2 phenotypes; yet, noticeable plasticity allows them to dynamically shift between several distinct functional subtypes. In atherosclerosis, low-density lipoprotein (LDL)-derived cholesterol accumulates within macrophages as cytoplasmic lipid droplets thereby generating macrophage foam cells, which are involved in all steps of atherosclerosis. The conversion of macrophages into foam cells may suppress the expression of given proinflammatory genes and thereby initiate their transcriptional reprogramming toward an anti-inflammatory phenotype. In this particular sense, foam cell formation can be considered anti-atherogenic. The tumor-associated macrophages (TAMs) may become polarized into anti-tumoral M1 and pro-tumoral M2 phenotypes. Mechanistically, the TAMs can regulate the survival and proliferation of the surrounding cancer cells and participate in various aspects of tumor formation, progression, and metastasis. The TAMs may accumulate lipids, but their type and their specific roles in tumorigenesis are still poorly understood. Here, we discuss how the phenotypic and functional plasticity of macrophages allows their multifunctional response to the distinct microenvironments in developing atherosclerotic lesions and in developing malignant tumors. We also discuss how the inflammatory reactions of the macrophages may influence the development of atherosclerotic plaques and malignant tumors, and highlight the potential therapeutic effects of targeting lipid-laden macrophages in either disease.
publishDate 2022
dc.date.none.fl_str_mv 2
2022-01-01
2022
2022-01-01
dc.type.none.fl_str_mv Article de revisió
http://purl.org/coar/resource_type/c_dcae04bc
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://ddd.uab.cat/record/282319
https://dx.doi.org/urn:doi:10.3389/fcvm.2022.777822
url https://ddd.uab.cat/record/282319
https://dx.doi.org/urn:doi:10.3389/fcvm.2022.777822
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.relation.none.fl_str_mv Instituto de Salud Carlos III https://doi.org/10.13039/501100004587 PI1900136
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
https://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:Dipòsit Digital de Documents de la UAB
instname:Universitat Autònoma de Barcelona
instname_str Universitat Autònoma de Barcelona
reponame_str Dipòsit Digital de Documents de la UAB
collection Dipòsit Digital de Documents de la UAB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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