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Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation

Cardiovascular diseases, the notorious killer, are mainly caused by atherosclerosis (AS) characterized by lipids, cholesterol, and iron overload in plaques. Macrophages are effector cells and accumulate to the damaged and inflamed sites of arteries to internalize native and chemically modified lipop...

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Autores principales: Li, Hongxia, Cao, Zhiqiang, Wang, Lili, Liu, Chang, Lin, Hongkun, Tang, Yuhan, Yao, Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9007036/
https://www.ncbi.nlm.nih.gov/pubmed/35432323
http://dx.doi.org/10.3389/fimmu.2022.843712
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author Li, Hongxia
Cao, Zhiqiang
Wang, Lili
Liu, Chang
Lin, Hongkun
Tang, Yuhan
Yao, Ping
author_facet Li, Hongxia
Cao, Zhiqiang
Wang, Lili
Liu, Chang
Lin, Hongkun
Tang, Yuhan
Yao, Ping
author_sort Li, Hongxia
collection PubMed
description Cardiovascular diseases, the notorious killer, are mainly caused by atherosclerosis (AS) characterized by lipids, cholesterol, and iron overload in plaques. Macrophages are effector cells and accumulate to the damaged and inflamed sites of arteries to internalize native and chemically modified lipoproteins to transform them into cholesterol-loaded foam cells. Foam cell formation is determined by the capacity of phagocytosis, migration, scavenging, and the features of phenotypes. Macrophages are diverse, and the subsets and functions are controlled by their surrounding microenvironment. Generally, macrophages are divided into classically activated (M1) and alternatively activated (M2). Recently, intraplaque macrophage phenotypes are recognized by the stimulation of CXCL4 (M4), oxidized phospholipids (Mox), hemoglobin/haptoglobin complexes [HA-mac/M(Hb)], and heme (Mhem). The pro-atherogenic or anti-atherosclerotic phenotypes of macrophages decide the progression of AS. Besides, apoptosis, necrosis, ferroptosis, autophagy and pyrotopsis determine plaque formation and cardiovascular vulnerability, which may be associated with macrophage polarization phenotypes. In this review, we first summarize the three most popular hypotheses for AS and find the common key factors for further discussion. Secondly, we discuss the factors affecting macrophage polarization and five types of macrophage death in AS progression, especially ferroptosis. A comprehensive understanding of the cellular and molecular mechanisms of plaque formation is conducive to disentangling the candidate targets of macrophage-targeting therapies for clinical intervention at various stages of AS.
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spelling pubmed-90070362022-04-14 Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation Li, Hongxia Cao, Zhiqiang Wang, Lili Liu, Chang Lin, Hongkun Tang, Yuhan Yao, Ping Front Immunol Immunology Cardiovascular diseases, the notorious killer, are mainly caused by atherosclerosis (AS) characterized by lipids, cholesterol, and iron overload in plaques. Macrophages are effector cells and accumulate to the damaged and inflamed sites of arteries to internalize native and chemically modified lipoproteins to transform them into cholesterol-loaded foam cells. Foam cell formation is determined by the capacity of phagocytosis, migration, scavenging, and the features of phenotypes. Macrophages are diverse, and the subsets and functions are controlled by their surrounding microenvironment. Generally, macrophages are divided into classically activated (M1) and alternatively activated (M2). Recently, intraplaque macrophage phenotypes are recognized by the stimulation of CXCL4 (M4), oxidized phospholipids (Mox), hemoglobin/haptoglobin complexes [HA-mac/M(Hb)], and heme (Mhem). The pro-atherogenic or anti-atherosclerotic phenotypes of macrophages decide the progression of AS. Besides, apoptosis, necrosis, ferroptosis, autophagy and pyrotopsis determine plaque formation and cardiovascular vulnerability, which may be associated with macrophage polarization phenotypes. In this review, we first summarize the three most popular hypotheses for AS and find the common key factors for further discussion. Secondly, we discuss the factors affecting macrophage polarization and five types of macrophage death in AS progression, especially ferroptosis. A comprehensive understanding of the cellular and molecular mechanisms of plaque formation is conducive to disentangling the candidate targets of macrophage-targeting therapies for clinical intervention at various stages of AS. Frontiers Media S.A. 2022-03-30 /pmc/articles/PMC9007036/ /pubmed/35432323 http://dx.doi.org/10.3389/fimmu.2022.843712 Text en Copyright © 2022 Li, Cao, Wang, Liu, Lin, Tang and Yao https://creativecommons.org/licenses/by/4.0/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.
spellingShingle Immunology
Li, Hongxia
Cao, Zhiqiang
Wang, Lili
Liu, Chang
Lin, Hongkun
Tang, Yuhan
Yao, Ping
Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation
title Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation
title_full Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation
title_fullStr Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation
title_full_unstemmed Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation
title_short Macrophage Subsets and Death Are Responsible for Atherosclerotic Plaque Formation
title_sort macrophage subsets and death are responsible for atherosclerotic plaque formation
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9007036/
https://www.ncbi.nlm.nih.gov/pubmed/35432323
http://dx.doi.org/10.3389/fimmu.2022.843712
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