Cited by 409Cardiac Fibrosis and RemodelingAtherosclerosis and Cardiovascular DiseasesMesenchymal stem cell research

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Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction

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Ma, Yonggang, Mouton, Alan J., Lindsey, Merry L.·2018·Translational Research

DOI 10.1016/j.trsl.2017.10.001PMC PMC5846093

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Abstract

Macrophages play critical roles in homeostatic maintenance of the myocardium under normal conditions and in tissue repair after injury. In the steady-state heart, resident cardiac macrophages remove senescent and dying cells and facilitate electrical conduction. In the aging heart, the shift in macrophage phenotype to a proinflammatory subtype leads to inflammaging. Following myocardial infarction (MI), macrophages recruited to the infarct produce both proinflammatory and anti-inflammatory mediators (cytokines, chemokines, matrix metalloproteinases, and growth factors), phagocytize dead cells, and promote angiogenesis and scar formation. These diverse properties are attributed to distinct macrophage subtypes and polarization status. Infarct macrophages exhibit a proinflammatory M1 phenotype early and become polarized toward an anti-inflammatory M2 phenotype later post-MI. Although this classification system is oversimplified and needs to be refined to accommodate the multiple different macrophage subtypes that have been recently identified, general concepts on macrophage roles are independent of subtype classification. This review summarizes current knowledge about cardiac macrophage origins, roles, and phenotypes in the steady state, with aging, and after MI, as well as highlights outstanding areas of investigation.

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Authors: Ma, Y., Mouton, A. J., & Lindsey, M. L.
Affiliations: University of Mississippi Medical Center (US)
Corresponding author: Lindsey, Merry L.
ORCID: Ma, Yonggang
Mouton, Alan J.
Lindsey, Merry L.
Venue: Translational Research
Publisher: Elsevier BV
Published: 2018-01
Volume: 191
Pages: 15-28
ISSN: 1878-1810 (ISSN-L)
1931-5244
DOI: 10.1016/j.trsl.2017.10.001
PMC: PMC5846093
OpenAlex: W2763341318
Cited by: 405
References: 143
Citations by year: 2026: 34 · 2025: 27 · 2024: 64 · 2023: 73 · 2022: 49 · 2021: 50 · 2020: 55 · 2019: 32 · 2018: 21
FWCI: 4.19
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Locations: Translational research (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
PubMed Central (acceptedVersion, cc-by-nc-nd)
Funders: American Heart Association (15SDG22930009)
National Institutes of Health (GM104357, GM114833, HL051971, HL129823, HL075360, HL105324, GM115428)
Biomedical Laboratory Research and Development, VA Office of Research and Development (5I01BX000505)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Mesenchymal stem cell research
Keywords: cardiac macrophages, macrophage polarization, M1/M2 macrophages, myocardial infarction, cardiac aging, inflammaging, tissue homeostasis, phagocytosis, angiogenesis, scar formation, macrophage origin, macrophage phenotype
MeSH terms: Aging, Heart, Humans, Macrophages, Myocardial Infarction, Myocardium, Biomarkers

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Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction

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