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

Ma, Yonggang; Mouton, Alan J.; Lindsey, Merry L.

doi:10.1016/j.trsl.2017.10.001

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

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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In the aging heart, macrophages recruited to the site of infarction exhibit a pro-inflammatory M1 phenotype initially and subsequently transition to an anti-inflammatory M2 phenotype after myocardial infarction.
“However, in the aging heart, macrophages recruited to the site of infarction exhibit a pro-inflammatory M1 phenotype initially, but subsequently transition to an anti-inflammatory M2 phenotype after myocardial infarction (MI).”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [143]
The Abstract and “Macrophages in the MI Heart—Macrophage phenotypes” describe an early M1 and later M2 pattern after infarction. But the paper treats aging-heart macrophages separately and does not establish that this post-MI pattern occurs specifically in aging hearts. Its “Macrophage polarization mechanisms” section also says whether individual macrophages convert in vivo remains uncertain. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measured
The M1-to-M2 phenotypic switch of macrophages after myocardial infarction promotes angiogenesis and scar formation, aiding recovery.
“This phenotypic switch promotes angiogenesis and scar formation, aiding in the recovery process.143”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [143]

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SPOTLIGHT REVIEW Cardiacmacrophages and their role in ischaemic heart disease
Frantz, S., & Nahrendorf, M. (2016)

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
Health Sciences › Medicine › Genetics › 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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