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Abandoning M1/M2 for a Network Model of Macrophage Function
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“Although macrophages have traditionally been classified as either classically-activated (M1) or alternatively-activated (M2), it is now recognised that they exist along a continuum of activation states 8 , with M1 and M2 representing the prototypical pro-and anti-inflammatory extremes of this spectrum 9 .”
From Soft tissue-mimicking hydrogel stiffness modulates polarisation of human monocyte-derived macrophages (2025) · cites this paper as [9]
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Metadata
- Authors
- Nahrendorf, M., & Swirski, F. K.
- Affiliations
- Harvard University (US)
- From the Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston.
- ORCID
- Nahrendorf, Matthias
- Venue
- Circulation Research
- Published
- 2016-07-22
- Volume
- 119
- Issue
- 3
- Pages
- 414-417
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC4965179
- OpenAlex
- W2505661818
- Cited by
- 525
- References
- 41
- Citations by year
- 2026: 59 · 2025: 63 · 2024: 54 · 2023: 74 · 2022: 60 · 2021: 75 · 2020: 53 · 2019: 35 · 2018: 35 · 2017: 16 · 2016: 1
- FWCI
- 2.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (HL128264)
- National Heart, Lung, and Blood Institute (R01HL117829, R01HL095629, R01HL128264, R01HL096576, R01HL095612)
- National Institute of Neurological Disorders and Stroke (R01NS084863)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- macrophage polarization, M1/M2 macrophages, network models, macrophage function, macrophage heterogeneity
- MeSH terms
- Animals, Humans, Macrophages, Models, Biological, Myocardial Infarction, Macrophage-1 Antigen, Galectin 3
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