ArticleFrontiers in immunology2011
Molecular mechanisms regulating macrophage response to hypoxia.
Article in Frontiers in immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Immune cells in keloids: mechanisms and potential treatments.Annals of medicine · 2026Review
- Review
- Article
- Polarized Macrophages Show Diverse Pro-Angiogenic Characteristics Under Normo- and Hyperglycemic Conditions.International journal of molecular sciences · 2025Article
- Inflammatory stimuli and hypoxia on atherosclerotic plaque thrombogenicity: Linking macrophage tissue factor and glycolysis.PloS one · 2025Article
- Hypoxia represses pattern-triggered immune responses in Arabidopsis.Plant physiology · 2024Article
- A Hypoxia-Decidual Macrophage Regulatory Axis in Normal Pregnancy and Spontaneous Miscarriage.International journal of molecular sciences · 2024Review
- Distinct hypoxia-induced translational profiles of embryonic and adult-derived macrophages.iScience · 2023Article
- HIV Promotes Neurocognitive Impairment by Damaging the Hippocampal Microvessels.Molecular neurobiology · 2022Article
- Hypoxia Inhibits Subretinal Inflammation Resolution Thrombospondin-1 Dependently.International journal of molecular sciences · 2022Article
- Article
- External cervical resorption detected via cone-beam computed tomography in a patient with myelin oligodendrocyte glycoprotein antibody-associated disease: A case report.Clinical case reports · 2021Article
- Review
- Hypoxia-induced alternative splicing: the 11th Hallmark of Cancer.Journal of experimental & clinical cancer research : CR · 2020Review
- Chemokine receptor 5 blockade modulates macrophage trafficking in renal ischaemic-reperfusion injury.Journal of cellular and molecular medicine · 2020Article
- Multiplatform Molecular Profiling Reveals Epigenomic Intratumor Heterogeneity in Ependymoma.Cell reports · 2020Article
- A mechanistic integrative computational model of macrophage polarization: Implications in human pathophysiology.PLoS computational biology · 2019Article
- Hyperglycemia acts in synergy with hypoxia to maintain the pro-inflammatory phenotype of macrophages.PloS one · 2019Article
- Hypoxia restrains the expression of complement component 9 in tumor-associated macrophages promoting non-small cell lung cancer progression.Cell death discovery · 2018Article
- Function of miR-146a-5p in Tumor Cells As a Regulatory Switch between Cell Death and Angiogenesis: Macrophage Therapy Revisited.Frontiers in immunology · 2017Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monocytes and Macrophages (Mo/Mɸ) exhibit great plasticity, as they can shift between different modes of activation and, driven by their immediate microenvironment, perform divergent functions. These include, among others, patrolling their surroundings and maintaining homeostasis (resident Mo/Mɸ), combating invading pathogens and tumor cells (classically activated or M1 Mo/Mɸ), orchestrating wound healing (alternatively activated or M2 Mo/Mɸ), and restoring homeostasis after an inflammatory response (resolution Mɸ). Hypoxia is an important factor in the Mɸ microenvironment, is prevalent in many physiological and pathological conditions, and is interdependent with the inflammatory response. Although Mo/Mɸ have been studied in hypoxia, the mechanisms by which hypoxia influences the different modes of their activation, and how it regulates the shift between them, remain unclear. Here we review the current knowledge about the molecular mechanisms that mediate this hypoxic regulation of Mɸ activation. Much is known about the hypoxic transcriptional regulatory network, which includes the master regulators hypoxia-induced factor-1 and NF-κB, as well as other transcription factors (e.g., AP-1, Erg-1), but we also highlight the role of post-transcriptional and post-translational mechanisms. These mechanisms mediate hypoxic induction of Mɸ pro-angiogenic mediators, suppress M1 Mɸ by post-transcriptionally inhibiting pro-inflammatory mediators, and help shift the classically activated Mɸ into an activation state which approximate the alternatively activated or resolution Mɸ.
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