Macrophages: master regulators of inflammation and fibrosis
Open accessAbstract
Macrophages are found in close proximity with collagen-producing myofibroblasts and indisputably play a key role in fibrosis. They produce profibrotic mediators that directly activate fibroblasts, including transforming growth factor-beta1 and platelet-derived growth factor, and control extracellular matrix turnover by regulating the balance of various matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases. Macrophages also regulate fibrogenesis by secreting chemokines that recruit fibroblasts and other inflammatory cells. With their potential to act in both a pro- and antifibrotic capacity, as well as their ability to regulate the activation of resident and recruited myofibroblasts, macrophages and the factors they express are integrated into all stages of the fibrotic process. These various, and sometimes opposing, functions may be performed by distinct macrophage subpopulations, the identification of which is a growing focus of fibrosis research. Although collagen-secreting myofibroblasts once were thought of as the master "producers" of fibrosis, this review will illustrate how macrophages function as the master "regulators" of fibrosis.
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Restorative macrophages are characterized by enhanced efferocytosis, reduced pro-inflammatory signaling, and increased matrix degradation capacity.
“In any case, pro-resolution macrophages are functionally characterised by enhanced clearance of apoptotic cells, increased secretion of fibrolytic enzymes such as MMPs and cathepsins, and reduced pro-inflammatory signalling, thus promoting fibrosis resolution (95, 96).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [95]
The section ‘A Role for Macrophages in the Resolution and Reversal of Fibrosis’ (page unavailable) links fibrosis resolution to macrophage clearance of apoptotic cells and production of ECM-degrading MMPs. The phagocytosis section says engulfing apoptotic cells typically represses inflammation. Our copy does not establish this three-part profile as a defined pro-resolution phenotype or identify cathepsins as the fibrolytic enzymes involved. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPro-resolution macrophages are functionally characterised by enhanced clearance of apoptotic cells, increased secretion of fibrolytic enzymes such as MMPs and cathepsins, and reduced pro-inflammatory signalling, thus promoting fibrosis resolution.
“In any case, pro-resolution macrophages are functionally characterised by enhanced clearance of apoptotic cells, increased secretion of fibrolytic enzymes such as MMPs and cathepsins, and reduced pro-inflammatory signalling, thus promoting fibrosis resolution (95, 96).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [95]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMacrophages play a central role in regulating liver fibrosis.
“The central role of macrophages in regulating liver fibrosis is now well recognized11,23.”
From Hepatocyte mitochondria-derived danger signals directly activate hepatic stellate cells and drive progression of liver fibrosis (2020) · cites this paper as [11]
Prolonged inflammation and remodeling can lead to fibrosis or hypertrophic scar formation due to dysregulation of the default healing process.
“In some cases, as will be discussed in further detail, prolonged inflammation and remodeling leading to fibrosis or hypertrophic scar formation may occur due to dysregulation of the default healing process [32,86,101,102].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [101]
Persistent or dysregulated inflammation can result in fibrosis following tissue injury or infection.
“Persistent or dysregulated inflammation can result in fibrosis following tissue injury or in the setting of infection [101,102].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [101]
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- Authors
- Wynn, T., & Barron, L.
- Affiliations
- National Institutes of Health (US)
- Venue
- Seminars in Liver Disease
- Publisher
- Georg Thieme Verlag KG
- Published
- 2010-07-21
- Volume
- 30
- Issue
- 03
- Pages
- 245-257
- ISSN
- 0272-8087 (ISSN-L)
- 1098-8971
- PMC
- PMC2924662
- OpenAlex
- W2032639324
- Cited by
- 1,392
- References
- 177
- Citations by year
- 2026: 65 · 2025: 80 · 2024: 110 · 2023: 108 · 2022: 85 · 2021: 116 · 2020: 122 · 2019: 107 · 2018: 86 · 2017: 78 · 2016: 93 · 2015: 94 · 2014: 79 · 2013: 64 · 2012: 62
- FWCI
- 34.67
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Seminars in Liver Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (ZIAAI001019, ZIAAI000829)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Keywords
- macrophages, fibrosis, inflammation, myofibroblasts, TGF-β1, platelet-derived growth factor, matrix metalloproteinases, tissue inhibitors of metalloproteinases, extracellular matrix turnover, chemokines, macrophage subpopulations, liver fibrosis
- MeSH terms
- Animals, Arginase, Extracellular Matrix, Hepatitis, Humans, Liver, Liver Cirrhosis, Macrophage Activation, Macrophages, Phagocytosis, Signal Transduction, Cytokines, Inflammation Mediators, Transforming Growth Factor beta1, Hepatic Stellate Cells
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