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Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction
Open accessAbstract
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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“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]
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“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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Myocardial Infarction Superimposed on Aging: MMP-9 Deletion Promotes M2 Macrophage Polarization
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Self-citationImmune Modulation of Cardiac Repair and Regeneration: The Art of Mending Broken Hearts
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- Pawelec, 1999, Immunosenescence: impact in the young as well as the old?, Mech Ageing Dev, 108, 1
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Inflammation and aging: signaling pathways and intervention therapies
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Metadata
- Authors
- Ma, Y., Mouton, A. J., & Lindsey, M. L.
- Affiliations
- University of Mississippi Medical Center (US)
- Corresponding author
- Lindsey, Merry L.
- Venue
- Translational Research
- Publisher
- Elsevier BV
- Published
- 2018-01
- Volume
- 191
- Pages
- 15-28
- ISSN
- 1878-1810 (ISSN-L)
- 1931-5244
- 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
- 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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