Hypoxia Regulates Macrophage Functions in Inflammation
Open accessAbstract
The presence of areas of hypoxia is a prominent feature of various inflamed, diseased tissues, including malignant tumors, atherosclerotic plaques, myocardial infarcts, the synovia of joints with rheumatoid arthritis, healing wounds, and sites of bacterial infection. These areas form when the blood supply is occluded and/or unable to keep pace with the growth and/or infiltration of inflammatory cells in a given area. Macrophages are present in all tissues of the body where they normally assist in guarding against invading pathogens and regulate normal cell turnover and tissue remodeling. However, they are also known to accumulate in large numbers in such ischemic/hypoxic sites. Recent studies show that macrophages then respond rapidly to the hypoxia present by altering their expression of a wide array of genes. In the present study, we outline and compare the phenotypic responses of macrophages to hypoxia in different diseased states and the implications of these for their progression and treatment.
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Hypoxia plays a pivotal role in TAM recruitment by directing macrophage chemotaxis into the tumor core through secretion of chemokines such as CCL2, HIF-1α, HIF-2α, and endothelin-2.
“Hypoxia, a hallmark of advanced malignancies, plays a pivotal role in TAM recruitment. Hypoxic tumor cells secrete chemokines (e.g., CCL2), hypoxia-inducible factors (HIF-1α, HIF-2α), and endothelin-2, which direct macrophage chemotaxis into the tumor core [66].”
From Modeling Tumor Microenvironment Complexity In Vitro: Spheroids as Physiologically Relevant Tumor Models and Strategies for Their Analysis (2025) · cites this paper as [66]
The Malignant tumors section says TAMs accumulate in hypoxic tumor areas partly because tumor and/or stromal cells release chemoattractants, including endothelin 2. It also names CCL2 as a tumor-derived recruiter of monocytes, but does not say hypoxia induces its secretion. The section says macrophages up-regulate HIF-1 and HIF-2 in hypoxic areas, not that tumor cells secrete them to direct chemotaxis into the tumor core; page numbers were not supplied for these passages. (LLM, conf=0.89)
Experimental — accuracy not yet measuredMacrophages accumulate in hypoxic environments to release prohealing and pro-angiogenic factors such as VEGF, PDGF and enzymes such as COX2.
“Macrophages accumulate in hypoxic environments to release prohealing and pro-angiogenic factors such as vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF) [63] and enzymes such as Cyclooxygenase 2 (COX2) [64].”
From Biomaterial based modulation of macrophage polarization: a review and suggested design principles (2015) · cites this paper as [63]
Macrophage-secreted growth factors such as VEGF, VEGFR1, VEGFR2, PDGF, FGF, and TGF-β are induced by hypoxia.
“Macrophage-secreted growth factors such as vascular endothelial growth factor (VEGF) and its receptor VEGFR1 and VEGFR2, platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), and transforming growth factor-β (TGF-β) have been reported to be induced by hypoxia [76,77,78].”
From The Pathogenesis of Adenomyosis vis-à-vis Endometriosis (2020) · cites this paper as [76]
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- Authors
- Murdoch, C., Muthana, M., & Lewis, C. E.
- Affiliations
- University of Sheffield (GB)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-11
- Volume
- 175
- Issue
- 10
- Pages
- 6257-6263
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2095800957
- Cited by
- 455
- References
- 87
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 14 · 2023: 15 · 2022: 26 · 2021: 18 · 2020: 16 · 2019: 11 · 2018: 27 · 2017: 33 · 2016: 16 · 2015: 30 · 2014: 29 · 2013: 34 · 2012: 22
- FWCI
- 1.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- Directorate for Biological Sciences
- Medical Research Council
- Engineering and Physical Sciences Research Council
- Biotechnology and Biological Sciences Research Council
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- hypoxia, macrophages, inflammation, ischemia, gene expression regulation, macrophage phenotype, tumor hypoxia, atherosclerosis, myocardial infarction, rheumatoid arthritis, wound healing, bacterial infection, tissue remodeling
- MeSH terms
- Animals, Hypoxia, Arthritis, Rheumatoid, Bacterial Infections, Humans, Inflammation, Macrophages, Neoplasms, Wounds and Injuries, Cell Hypoxia, Gene Expression, Models, Immunological, Atherosclerosis, Mice, In Vitro Techniques
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