ArticlePloS one2012
Hypoxia enhances the proliferative response of macrophages to CSF-1 and their pro-survival response to TNF.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Macrophage Hypoxia Signaling Pathways and Their Roles in Sepsis.Journal of inflammation research · 2026Review
- Integrative single-cell and spatial transcriptome analysis reveals the functions of TREM2Molecular and cellular biochemistry · 2025Article
- Hyperthermia Influences the Secretion Signature of Tumor Cells and Affects Endothelial Cell Sprouting.Biomedicines · 2023Article
- Cellular metabolic adaptations in rheumatoid arthritis and their therapeutic implications.Nature reviews. Rheumatology · 2022Review
- Macrophages and Cardiovascular Health.Physiological reviews · 2018Review
- Oxygen ultra-fine bubbles water administration prevents bone loss of glucocorticoid-induced osteoporosis in mice by suppressing osteoclast differentiation.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2017Article
- Anti-colony-stimulating factor therapies for inflammatory and autoimmune diseases.Nature reviews. Drug discovery · 2016Review
- Hypoxia, mitochondrial dysfunction and synovial invasiveness in rheumatoid arthritis.Nature reviews. Rheumatology · 2016Review
- Celastrol protects ischaemic myocardium through a heat shock response with up-regulation of haeme oxygenase-1.British journal of pharmacology · 2014Article
- mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity.Science (New York, N.Y.) · 2014Article
- Positive correlation of STAT1 and miR-146a with anemia in patients with systemic lupus erythematosus.Journal of clinical immunology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In chronic inflammatory lesions there are increased numbers of macrophages with a possible contribution of enhanced survival/proliferation due, for example, to cytokine action; such lesions are often hypoxic. Prior studies have found that culture in low oxygen can promote monocyte/macrophage survival. We show here, using pharmacologic inhibitors, that the hypoxia-induced pro-survival response of macrophages exhibits a dependence on PI3-kinase and mTOR activities but surprisingly is suppressed by Akt and p38 MAPK activities. It was also found that in hypoxia at CSF-1 concentrations, which under normoxic conditions are suboptimal for macrophage proliferation, macrophages can proliferate more strongly with no evidence for alteration in CSF-1 receptor degradation kinetics. TNF promoted macrophage survival in normoxic conditions with an additive effect in hypoxia. The enhanced hypoxia-dependent survival and/or proliferation of macrophages in the presence of CSF-1 or TNF may contribute to their elevated numbers at a site of chronic inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.